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        <title>Heart Failure Reviews via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Heart Failure Reviews' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Heart+Failure+Reviews&t=Heart+Failure+Reviews&s=Search&f=source]]></link>
        <lastBuildDate>Sat, 20 Mar 2010 13:55:52 +0100</lastBuildDate>
        <item>
            <title>Stem cells for heart failure in the aging heart</title>
            <link>http://www.medworm.com/index.php?rid=3360418&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Faj08552540511724%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Despite a wide range of therapeutic interventions, the prognosis for most patients with heart failure remains poor. The identification
 of stem cells with the ability to generate cardiomyocytes and vascular cells and promote local repair and survival pathways
 has highlighted the ability of the heart to undergo regeneration and potentially provides a new therapeutic strategy for treatment
 of the failing heart. In recent years, however, clinical trials aimed at exploiting the beneficial effects of stem and progenitor
 cells to treat patients with cardiovascular disease have resulted in mild improvements at best, suggesting that these cells
 and/or the conditions in which they find themselves are not conducive to cardiac repair. Heart failure is most prevalent among
 old...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3360418</comments>
            <pubDate>Thu, 11 Mar 2010 18:24:42 +0100</pubDate>
            <guid isPermaLink="false">3360418</guid>        </item>
        <item>
            <title>The role of inflammatory and fibrogenic pathways in heart failure associated with aging</title>
            <link>http://www.medworm.com/index.php?rid=3355765&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fd342417k43702884%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Heart failure is strongly associated with aging. Elderly patients with heart failure often have preserved systolic function
 exhibiting left ventricular hypertrophy accompanied by a decline in diastolic function. Experimental studies have demonstrated
 that age-related cardiac fibrosis plays an important role in the pathogenesis of diastolic heart failure in senescent hearts.
 Reactive oxygen species and angiotensin II are critically involved in fibrotic remodeling of the aging ventricle; their fibrogenic
 actions may be mediated, at least in part, through transforming growth factor (TGF)-β. The increased prevalence of heart failure
 in the elderly is also due to impaired responses of the senescent heart to cardiac injury. Aging is associated with suppressed
 inflammat...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3355765</comments>
            <pubDate>Wed, 10 Mar 2010 16:17:30 +0100</pubDate>
            <guid isPermaLink="false">3355765</guid>        </item>
        <item>
            <title>The epidemiology and management of elderly patients with myocardial infarction or heart failure</title>
            <link>http://www.medworm.com/index.php?rid=3355764&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fw00ggp55g72t1t31%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Heart disease is important in elderly patients. The treatment of myocardial infarction and heart failure are particularly
 important and will continue to play an important role across the globe. Advances in treatment of myocardial infarction have
 made tremendous inroads in the short and long term survival of patients, young and old, however, many currently employed strategies
 have not been tested in patients who are elderly, who paradoxically, form a growing subset of patients with heart disease.
 A similar paradigm exists in heart failure for both diagnosis and treatment. Attention to this issue is important when selecting
 treatment strategies and a focus on the goals of care is critical when decisions for care must be undertaken.
 
 
	Content Type Journal ArticleDO...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3355764</comments>
            <pubDate>Wed, 10 Mar 2010 16:17:30 +0100</pubDate>
            <guid isPermaLink="false">3355764</guid>        </item>
        <item>
            <title>Is adiponectin a bystander or a mediator in heart failure? The tangled thread of a good-natured adipokine in aging and cardiovascular disease</title>
            <link>http://www.medworm.com/index.php?rid=3355766&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F54028752274l4178%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Adiponectin is an adipose tissue-derived adipokine abundant in human plasma. Increasing evidence from experimental studies
 suggests that adiponectin plays a protective role in the cardiovascular system. However, epidemiological studies revealed
 that high levels of adiponectin were associated with increased mortality and severity of congestive heart failure. Furthermore,
 several prospective studies indicated that high levels of adiponectin were positively correlated with increased total and
 cardiovascular disease mortality in the elderly. These results are completely opposite to our expectation based on the beneficial
 effects of adiponectin. Clinical observations demonstrated that plasma adiponectin levels were positively associated with
 B-type natriuretic peptide ...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3355766</comments>
            <pubDate>Wed, 10 Mar 2010 16:17:29 +0100</pubDate>
            <guid isPermaLink="false">3355766</guid>        </item>
        <item>
            <title>Role of osteopontin in heart failure associated with aging</title>
            <link>http://www.medworm.com/index.php?rid=3240976&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fp3242g608g035011%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Cardiovascular disease is one of the leading causes of death in the elderly. Much of the morbidity and mortality in the elderly
 is attributable to acute ischemic events leading to myocardial infarction (MI) and death of cardiac myocytes. Evidence has
 been provided that aging associated with adverse remodeling post MI as demonstrated by less effective myocardial repair, greater
 infarct expansion, and septal hypertrophy. Expression of osteopontin (OPN) increases in the heart post MI. Transgenic mice
 studies suggest that increased expression of OPN plays a protective role in post-MI LV remodeling by modulating collagen deposition
 and fibrosis. OPN, a multifunctional protein, has the potential to influence the molecular and cellular changes associated
 with infarct hea...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240976</comments>
            <pubDate>Tue, 02 Feb 2010 17:51:25 +0100</pubDate>
            <guid isPermaLink="false">3240976</guid>        </item>
        <item>
            <title>Role and benefits of exercise in the management of patients with heart failure</title>
            <link>http://www.medworm.com/index.php?rid=3209632&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fb47188u823816454%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Initial research established the feasibility of exercise training in patients with heart failure, as well as associated physiological
 benefits. This review summarizes the findings from over two dozen single-site studies that address the effect of exercise
 training on exercise capacity and cardiovascular and peripheral function. In addition, it incorporates the results from two
 meta-analyses and a recently completed multi-center trial, all of which studied the effects of exercise training on clinical
 outcomes. The major conclusions from these studies are that exercise training is safe; improves health status and exercise
 capacity; helps attenuate much of the abnormal pathophysiology that develops with heart failure; and yields a modest reduction
 in clinical events....</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3209632</comments>
            <pubDate>Mon, 25 Jan 2010 17:01:05 +0100</pubDate>
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        <item>
            <title>Cardiomyopathy in Duchenne muscular dystrophy: pathogenesis and therapeutics</title>
            <link>http://www.medworm.com/index.php?rid=3040898&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F745v75961181px24%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Duchenne muscular dystrophy (DMD) is an X-linked recessive disorder caused by the absence of dystrophin, a sarcolemmal protein
 which links the cytoskeleton to the extracellular matrix by interacting with a large number of proteins. Heart failure is
 a classic complication of this disease. The authors review the pathogenesis and therapeutics of cardiac involvement in DMD.
 
	Content Type Journal ArticleDOI 10.1007/s10741-009-9156-8Authors
		Abdallah Fayssoil, University of Medicine and Dentistry of New Jersey Camden NJ USAOlivier Nardi, Raymond Poincaré Hospital, AP-HP Intensive Care Unit Garches FranceDavid Orlikowski, Raymond Poincaré Hospital, AP-HP Intensive Care Unit Garches FranceDjillali Annane, Raymond Poincaré Hospital, AP-HP Intensive Care Unit Garches Fran...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3040898</comments>
            <pubDate>Fri, 27 Nov 2009 07:06:28 +0100</pubDate>
            <guid isPermaLink="false">3040898</guid>        </item>
        <item>
            <title>George C. Sutton, Kanu Chatterjee: Heart failure: current clinical understanding</title>
            <link>http://www.medworm.com/index.php?rid=2996831&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fe7850u66221u0v76%2F</link>
            <description>Content Type Journal ArticleCategory Book ReviewDOI 10.1007/s10741-009-9155-9Authors
		Sidney Goldstein, Wayne State University Detroit MI USA
	

	
		Journal Heart Failure ReviewsOnline ISSN 1573-7322Print ISSN 1382-4147 (Source: Heart Failure Reviews)</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2996831</comments>
            <pubDate>Fri, 13 Nov 2009 18:28:44 +0100</pubDate>
            <guid isPermaLink="false">2996831</guid>        </item>
        <item>
            <title>Agents with inotropic properties for the management of acute heart failure syndromes. Traditional agents and beyond</title>
            <link>http://www.medworm.com/index.php?rid=2947879&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F0454480241703821%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Treatment with inotropic agents is one of the most controversial topics in heart failure. Initial enthusiasm, based on strong
 pathophysiological rationale and apparent empirical efficacy, has been progressively limited by results of controlled trials
 and registries showing poorer outcomes of the patients on inotropic therapy. The use of these agents remains, however, potentially
 indicated in a significant proportion of patients with low cardiac output, peripheral hypoperfusion and end-organ dysfunction
 caused by heart failure. Limitations of inotropic therapy seem to be mainly related to their mechanisms of action entailing
 arrhythmogenesis, peripheral vasodilation, myocardial ischemia and damage, and possibly due to their use in patients without
 a clear indicatio...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2947879</comments>
            <pubDate>Thu, 29 Oct 2009 19:51:20 +0100</pubDate>
            <guid isPermaLink="false">2947879</guid>        </item>
        <item>
            <title>Do we have two hearts? New insights in right ventricular function supported by myocardial imaging echocardiography</title>
            <link>http://www.medworm.com/index.php?rid=2944975&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fa85845x1jr061265%2F</link>
            <description>This article focuses on some of the challenges related to the assessment of RV function
 in the setting of the RV’s unique anatomic, physiologic, conventional and newer echocardiographic aspects, and therapeutic
 implications. The majority of proposed methods of echocardiographic assessment of RV function are based on volumetric approximations
 of the RV. Such approaches have inherent limitations, first as volume-related measures such as EF are load dependent, second
 because of the complex geometry of the RV. The issue of RV geometry is usually overcome using geometry-independent parameters
 such as tricuspid annular excursion and the Tei index. The recent introduction of real-time three-dimensional echocardiography
 and myocardial imaging echocardiography (tissue Doppler imaging, 1D-st...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2944975</comments>
            <pubDate>Thu, 29 Oct 2009 07:23:04 +0100</pubDate>
            <guid isPermaLink="false">2944975</guid>        </item>
        <item>
            <title>Potential of endothelin-1 and vasopressin antagonists for the treatment of congestive heart failure</title>
            <link>http://www.medworm.com/index.php?rid=2810719&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc8520pn66v3213gu%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;It is now becoming clear that two major systems namely the sympathetic nervous system and the renin-angiotensin system are
 activated in response to ischemic injury; these result in the elevation of plasma catecholamines and angiotensin II during
 the development of myocardial infarction as well as congestive heart failure. Although plasma levels of several other hormones
 including aldosterone, endothelin, vasopressin, natriuretic peptides, growth factors and inflammatory cytokines are also increased
 in heart failure, their relationship with changes in catecholamine and/or angiotensin levels as well as their significance
 for the induction of congestive heart failure are poorly understood. In this article we have examined the evidence regarding
 the role of endothelin...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2810719</comments>
            <pubDate>Fri, 18 Sep 2009 06:15:39 +0100</pubDate>
            <guid isPermaLink="false">2810719</guid>        </item>
        <item>
            <title>Architecture of the left ventricle: insights for optimal surgical ventricular restoration</title>
            <link>http://www.medworm.com/index.php?rid=2810720&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fq073162j71m68777%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The normal left ventricular shape has been defined as prolate ellipsoid. This shape is an adaptation to evolution. A knowledge
 of its unique macro and micro architecture forms the cornerstone in the understanding of its complex function. The left ventricle
 has a unique architecture with three different myofiber orientations, the longitudinal, circumferential and oblique fibers.
 The oblique orientation of fibers is essential for effective clockwise and anticlockwise torsional movements during systole
 and diastole, for optimal ventricular ejection and filling. The orientation and fiber angle decide the shape of the ventricle.
 An ellipsoid shape is vital for optimal function. Pathological disease states such as ischemic heart disease, valvular heart
 disease and cardi...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2810720</comments>
            <pubDate>Wed, 16 Sep 2009 12:56:36 +0100</pubDate>
            <guid isPermaLink="false">2810720</guid>        </item>
        <item>
            <title>Using patient DNA to optimize therapy in heart failure patients: a move toward perfection</title>
            <link>http://www.medworm.com/index.php?rid=2589479&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fyt1164202t140588%2F</link>
            <description>Content Type Journal ArticleDOI 10.1007/s10741-009-9150-1Authors
		Howard L. McLeod, University of North Carolina UNC Institute for Pharmacogenomics and Individualized Therapy, Division of Pharmacotherapy and Experimental Therapeutics, Division of Hematology and Oncology, and the Lineberger Comprehensive Cancer Center Campus Box 7360 Chapel Hill NC 27599 USA
	

	
		Journal Heart Failure ReviewsOnline ISSN 1573-7322Print ISSN 1382-4147 (Source: Heart Failure Reviews)</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2589479</comments>
            <pubDate>Mon, 06 Jul 2009 20:13:34 +0100</pubDate>
            <guid isPermaLink="false">2589479</guid>        </item>
        <item>
            <title>Role of guanylate cyclase modulators in decompensated heart failure</title>
            <link>http://www.medworm.com/index.php?rid=2564406&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fyq782724742267q6%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;In this review we investigate the role of particulate and soluble guanylate cyclase (pGC and sGC, respectively) pathways in
 heart failure, and several novel drugs that modify guanylate cyclase. Nesiritide and ularitide/urodilatin are natriuretic
 peptides with vasodilating, natriuretic and diuretic effects, acting on pGC, whilst cinaciguat (BAY 58-2667) is a novel sGC
 activator. Cinaciguat has a promising and novel mode of action because it can stimulate cyclic guanosine-3′,5′-monophosphate
 synthesis by targeting sGC in its nitric oxide-insensitive, oxidised ferric (Fe3+) or haem-free state. Thus, cinaciguat may also be effective under oxidative stress conditions resulting in oxidised or haem-free
 sGC refractory to traditional organic nitrate therapies. Prelimin...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2564406</comments>
            <pubDate>Wed, 01 Jul 2009 06:19:34 +0100</pubDate>
            <guid isPermaLink="false">2564406</guid>        </item>
        <item>
            <title>Why, when, and how to assess pulmonary congestion in heart failure: pathophysiological, clinical, and methodological implications</title>
            <link>http://www.medworm.com/index.php?rid=2464908&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fa733r173n158r553%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Acute heart failure syndrome (AHFS) is a major public health problem. It is defined as gradual or rapid change in heart failure
 (HF) signs and symptoms, which often results in an unplanned hospitalization and a need for urgent therapy. Many evidence-based
 pharmacologic, device, and surgical treatment for HF are available or under development. Despite these new treatments and
 improvement in survival, hospitalizations in HF have steadily increased over the last 30&amp;nbsp;years, and the post-discharge prognosis
 of patients hospitalized with AHFS remains poor (Gheorghiade et al. Circulation 112:3958–3968, 2005; Fonarow et al. Rev Cardiovasc
 Med 4:S21–30, 2003). Most hospitalizations for AHFS are related to “congestion” rather than to low cardiac output. The defin...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2464908</comments>
            <pubDate>Sun, 07 Jun 2009 09:03:22 +0100</pubDate>
            <guid isPermaLink="false">2464908</guid>        </item>
        <item>
            <title>Echocardiography in the assessment of left ventricular longitudinal systolic function: current methodology and clinical applications</title>
            <link>http://www.medworm.com/index.php?rid=2448886&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fa483583gn126k2uq%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Quantification of left ventricular (LV) systolic function represents a major aspect of echocardiographic assessment in the
 spectrum of cardiac diseases. However, because of the high complexity of LV contraction mechanics, the classical approach
 with assessment of a single measure of systolic function, such as ejection fraction or fractional shortening, has been largely
 superseded. During the last years, through the considerable technical advances in the field of ultrasonography, a number of
 different echocardiographic methodologies have become available to perform a detailed assessment of different aspects of LV
 contraction. In particular, evaluation of LV longitudinal systolic dynamics has progressively gained importance as a key aspect
 in the assessment of LV sy...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2448886</comments>
            <pubDate>Sat, 30 May 2009 07:49:09 +0100</pubDate>
            <guid isPermaLink="false">2448886</guid>        </item>
        <item>
            <title>Abnormalities of calcium metabolism and myocardial contractility depression in the failing heart</title>
            <link>http://www.medworm.com/index.php?rid=2418104&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ff40025x2q5516647%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Heart failure (HF) is characterized by molecular and cellular defects which jointly contribute to decreased cardiac pump function.
 During the development of the initial cardiac damage which leads to HF, adaptive responses activate physiological countermeasures
 to overcome depressed cardiac function and to maintain blood supply to vital organs in demand of nutrients. However, during
 the chronic course of most HF syndromes, these compensatory mechanisms are sustained beyond months and contribute to progressive
 maladaptive remodeling of the heart which is associated with a worse outcome. Of pathophysiological significance are mechanisms
 which directly control cardiac contractile function including ion- and receptor-mediated intracellular signaling pathways.
 Important...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2418104</comments>
            <pubDate>Tue, 12 May 2009 06:06:17 +0100</pubDate>
            <guid isPermaLink="false">2418104</guid>        </item>
        <item>
            <title>Introduction: biomarkers in heart failure</title>
            <link>http://www.medworm.com/index.php?rid=2399754&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc214005l05282127%2F</link>
            <description>Content Type Journal ArticleDOI 10.1007/s10741-009-9145-yAuthors
		Kirkwood F. Adams, University of North Carolina at Chapel Hill Departments of Medicine and Radiology, School of Medicine, UNC Heart Failure Program 730 Martin Luther King Jr Blvd Suite 207 Chapel Hill NC 27514 USA
	

	
		Journal Heart Failure ReviewsOnline ISSN 1573-7322Print ISSN 1382-4147 (Source: Heart Failure Reviews)</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2399754</comments>
            <pubDate>Thu, 07 May 2009 06:02:42 +0100</pubDate>
            <guid isPermaLink="false">2399754</guid>        </item>
        <item>
            <title>Multi-marker strategies in heart failure: clinical and statistical approaches</title>
            <link>http://www.medworm.com/index.php?rid=2391253&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fm00224k7587m927n%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Advances in genomics and proteomics promise to transform biomarker research, in which the major challenges will not be the
 discovery of new markers but rather the optimal selection and validation of a subgroup of clinically useful markers from the
 large pool of candidates. Critically, the value of new biomarkers panels will need to be assessed in the context of readily
 available clinical information in order to create more actionable knowledge rather than just greater complexity. Appropriate
 methodologies for the clinical and statistical evaluation of so called “multi-marker strategies” have not been systematically
 defined. Although specific criteria for the appropriate clinical and statistical evaluation of multi-marker strategies will
 vary based on the inten...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2391253</comments>
            <pubDate>Sun, 03 May 2009 05:49:45 +0100</pubDate>
            <guid isPermaLink="false">2391253</guid>        </item>
        <item>
            <title>Extracellular matrix fibrotic markers in heart failure</title>
            <link>http://www.medworm.com/index.php?rid=2383493&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fr2750682h78l584h%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Given the importance of fibrous tissue in leading to myocardial dysfunction, non-invasive assessment of fibrosis could prove
 a clinically useful tool in heart failure (HF) patients. Biomarkers may be used for early detection of otherwise subclinical
 disease, diagnostic assessment of an acute or chronic clinical syndrome, risk stratification of patients with a suspected
 or confirmed diagnosis, selection of an appropriate therapeutic intervention and monitoring the response to therapy. Extracellular
 matrix (ECM) biomarkers in HF are promising biomarkers. They are able to detect early changes in heart and large vessel structure
 and function and transition to HF. High ECM biomarker levels have been associated with poor outcome. The ability of treatment
 to reduce myoca...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2383493</comments>
            <pubDate>Thu, 30 Apr 2009 05:58:32 +0100</pubDate>
            <guid isPermaLink="false">2383493</guid>        </item>
        <item>
            <title>Systems biology and heart failure: concepts, methods, and potential research applications</title>
            <link>http://www.medworm.com/index.php?rid=2370592&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F1658484371843510%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Dramatic advances in molecular biology dominated twentieth century biomedical science and delineated the function of individual
 genes and molecules in exquisite detail. However, biological processes cannot be fully understood based on the properties
 of individual genes and molecules alone, since these elements act in concert to enable the specific functions that make for
 living cells and organisms. The discipline of systems biology provides a novel conceptual framework for understanding biological
 phenomenon. Systems biology synthesizes information concerning the interactions of genes and molecules and allows characterization
 of the supramolecular networks and functional modules that represent the most essential aspects of cell organization and physiology.
 
	Conte...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2370592</comments>
            <pubDate>Sun, 26 Apr 2009 05:48:39 +0100</pubDate>
            <guid isPermaLink="false">2370592</guid>        </item>
        <item>
            <title>Biomarker guided therapy for heart failure: focus on natriuretic peptides</title>
            <link>http://www.medworm.com/index.php?rid=2357788&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fyh70080650671607%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The management of heart failure remains challenging despite many therapeutic advances. Rigorous clinical trial evidence supports
 administration of multiple therapies, but utilization of evidence-based treatment remains inconsistent and suboptimal. Disease
 management programs appear effective, but remain costly and difficult to implement in today’s care system. Another approach
 involves optimizing therapy based on serial monitoring of cardiac biomarkers. Emerging results suggest that guiding therapy
 based on serial changes in natriuretic peptides may be an effective strategy. Although pilot work has provided encouraging
 results, appropriately designed, large-scale, prospective randomized trials are needed to confirm these preliminary findings
 and definitively est...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2357788</comments>
            <pubDate>Tue, 21 Apr 2009 04:41:34 +0100</pubDate>
            <guid isPermaLink="false">2357788</guid>        </item>
        <item>
            <title>Biomarkers of inflammation in heart failure</title>
            <link>http://www.medworm.com/index.php?rid=2332056&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F241821722ml6jq65%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Heart failure (HF) is characterized by the elaboration of a portfolio of pro-inflammatory cytokines and inflammatory mediators
 that are considered to contribute to disease progression by virtue of the deleterious effects that these molecules exert on
 the heart and circulation. Recent studies have suggested that these inflammatory mediators may serve as relevant markers of
 disease severity and HF prognosis. Moreover, there is evidence that changes in the levels of inflammatory biomarkers may prove
 useful in following the change in patient clinical status following institution of appropriate HF therapy. This review will
 focus on the emerging role of inflammatory biomarkers, including pro-inflammatory cytokines, C-reactive protein, and erythrocyte
 sedimentation rate ...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2332056</comments>
            <pubDate>Sun, 12 Apr 2009 06:02:11 +0100</pubDate>
            <guid isPermaLink="false">2332056</guid>        </item>
        <item>
            <title>Clinical applications of N-terminal pro B-type natriuretic peptide in heart failure and other cardiovascular diseases</title>
            <link>http://www.medworm.com/index.php?rid=2332057&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj4038n616040g023%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;N-terminal fragment of pro B-type natriuretic peptide (NT-proBNP) has emerged as an important adjunct in the management of
 heart failure (HF) and other cardiovascular diseases. NT-proBNP is a 76-amino acid peptide created during cleavage of the
 precursor molecule, Pro B-type natriuretic peptide (ProBNP). NT-proBNP is of significant diagnostic value in patients presenting
 with possible HF and is an important prognostic factor in this condition and other cardiovascular diseases. Ongoing research
 supports the potential value of this biomarker in non-cardiovascular disease. This review will describe clinical applications
 of NT-proBNP in HF and a broad range of other conditions.
 
	Content Type Journal ArticleDOI 10.1007/s10741-009-9142-1Authors
		Da-Rong Pu, The Second...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2332057</comments>
            <pubDate>Fri, 10 Apr 2009 06:12:32 +0100</pubDate>
            <guid isPermaLink="false">2332057</guid>        </item>
        <item>
            <title>Utility of natriuretic peptide testing in the evaluation and management of acute decompensated heart failure</title>
            <link>http://www.medworm.com/index.php?rid=2332058&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fa510222528047412%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The B-type natriuretic peptide (BNP) and the amino-terminal fragment of proBNP (NT-proBNP) are increased in heart failure
 in proportion to severity of symptoms, degree of left ventricular dysfunction, and elevation of cardiac filling pressures.
 These natriuretic peptides (NPs) are increasingly used for diagnostic and prognostic purposes in acute heart failure. While
 NP levels on admission provide independent prognostic information, serial determinations during hospitalization and at discharge
 better reflect adequacy of treatment and prognosis. The addition of BNP and NT-proBNP to usual clinical decision making enhances
 detection of high-risk patients who need aggressive follow-up and adjustment of treatment.
 
	Content Type Journal ArticleDOI 10.1007/s10741-009-914...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2332058</comments>
            <pubDate>Fri, 10 Apr 2009 06:12:31 +0100</pubDate>
            <guid isPermaLink="false">2332058</guid>        </item>
        <item>
            <title>Perspective on the clinical application of troponin in heart failure and states of cardiac injury</title>
            <link>http://www.medworm.com/index.php?rid=2332059&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh25h677u01544417%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The ability to measure the appearance of cardiac specific forms of troponin in the blood represents a major advance in the
 clinical assessment of patients with many types of cardiovascular disease, especially acute coronary syndromes. In this review
 we focus on the utility of troponin in heart failure where this biomarker has emerged as an independent predictor of prognosis
 providing information beyond clinical assessment and measurement of b-type natriuretic peptides. The novel clinical role of
 troponin in a variety of states associated with myocardial injury, including chemotherapy and patients with cardiovascular
 risk factors, is discussed.
 
	Content Type Journal ArticleDOI 10.1007/s10741-008-9124-8Authors
		Almasa Bass, UNC Heart Failure Program School of Phar...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2332059</comments>
            <pubDate>Sun, 05 Apr 2009 13:02:39 +0100</pubDate>
            <guid isPermaLink="false">2332059</guid>        </item>
        <item>
            <title>How does the heart (not) die? The role of autophagy in cardiomyocyte homeostasis and cell death</title>
            <link>http://www.medworm.com/index.php?rid=2221613&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F522m07v878167j31%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Autophagy plays a critical and seemingly dual-purposed role in cardiomyocytes, being implicated as a mechanism of both cellular
 survival, for example, during ischemia/reperfusion injury and a mechanism of cell death at stages in which progressive myocyte
 alterations are beyond repair. This review aims to highlight the current literature as it relates to autophagy in cardiomyocytes.
 It provides background into the mechanisms of cell death, discusses the details that are known about the ubiquitin proteasome
 system and autophagy, delves into the pathways that are known to initiate and inhibit autophagy, and comments on the role
 of autophagy in cardiomyocyte homeostasis and cell death.
 
	Content Type Journal ArticleDOI 10.1007/s10741-009-9137-yAuthors
		Pavittarpaul D...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2221613</comments>
            <pubDate>Wed, 25 Feb 2009 10:09:34 +0100</pubDate>
            <guid isPermaLink="false">2221613</guid>        </item>
        <item>
            <title>Istaroxime, a first in class new chemical entity exhibiting SERCA-2 activation and Na–K-ATPase inhibition: a new promising treatment for acute heart failure syndromes?</title>
            <link>http://www.medworm.com/index.php?rid=2215691&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Frw412751646r716t%2F</link>
            <description>In conclusion, istaroxime is a novel agent being investigated for the
 treatment of AHFS whose mechanism of action and cellular targets make it a promising therapy. Further studies with longer
 infusion times in patients with hypotension are required to confirm its efficacy and safety.
 
	Content Type Journal ArticleDOI 10.1007/s10741-009-9136-zAuthors
		Hashim Khan, Northwestern University, Feinberg School of Medicine Chicago IL USAMarco Metra, University of Brescia Department of Cardiology Brescia ItalyJohn E. A. Blair, Northwestern University, Feinberg School of Medicine Chicago IL USAMark Vogel, Northwestern University, Feinberg School of Medicine Chicago IL USAMatthew E. Harinstein, Northwestern University, Feinberg School of Medicine Chicago IL USAGerasimos S. Filippatos, University ...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2215691</comments>
            <pubDate>Tue, 24 Feb 2009 09:37:31 +0100</pubDate>
            <guid isPermaLink="false">2215691</guid>        </item>
        <item>
            <title>Cell delivery and tracking in post-myocardial infarction cardiac stem cell therapy: an introduction for clinical researchers</title>
            <link>http://www.medworm.com/index.php?rid=2215692&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F18214624224x828q%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Stem cell-based therapy for patients with post-infarct heart failure is a relatively new and revolutionary concept in cardiology.
 Despite the encouraging results from pre-clinical studies, outcomes from most clinical trials remain moderately positive while
 the clinical benefits are largely attributed to transplanted cell-associated paracrine effects in stimulating angiogenesis
 and protecting endogenous cardiomyocytes. This scenario indicates that there may be a considerably protracted iterative process
 of conceptual and procedural refinement before true clinical benefits can be fully materialized. At present, many pressing
 questions regarding cell therapy remain unanswered. In addition to the primary interest in determining the ideal type of stem
 cells with best c...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2215692</comments>
            <pubDate>Tue, 24 Feb 2009 09:37:29 +0100</pubDate>
            <guid isPermaLink="false">2215692</guid>        </item>
        <item>
            <title>A novel approach to improve cardiac performance: cardiac myosin activators</title>
            <link>http://www.medworm.com/index.php?rid=2209251&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc734206586n1wt0u%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Decreased systolic function is a central factor in the pathogenesis of heart failure, yet there are no safe medical therapies
 to improve cardiac function in patients. Currently available inotropes, such as dobutamine and milrinone, increase cardiac
 contractility at the expense of increased intracellular concentrations of calcium and cAMP, contributing to increased heart
 rate, hypotension, arrhythmias, and mortality. These adverse effects are inextricably linked to their inotropic mechanism
 of action. A new class of pharmacologic agents, cardiac myosin activators, directly targets the kinetics of the myosin head.
 In vitro studies have demonstrated that these agents increase the rate of effective myosin cross-bridge formation, increasing
 the duration and amount of m...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2209251</comments>
            <pubDate>Sat, 21 Feb 2009 08:11:08 +0100</pubDate>
            <guid isPermaLink="false">2209251</guid>        </item>
        <item>
            <title>Use of a new model of transgenic mice to clarify the respective functions of thyroid hormone receptors in vivo</title>
            <link>http://www.medworm.com/index.php?rid=3097817&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F503440v6k5645u61%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;3,5,3′-Triido-l-thyronine (T3) exerts pleiotropic actions on development and homeostasis mostly via its nuclear receptors, TRα1, TRβ1, and
 TRβ2, encoded by the THRA and THRB genes. Μouse genetics data outline the contrasting functions of THRA and THRB, and suggest
 that these are dictated by both the respective abundance of the receptor isoforms in a given cell type and the differences
 in the intrinsic properties of the receptors. The diversity of consequences of either hypothyroidism or THRA/THRB mutation
 is astonishing, suggesting that TR controls a large number of genes and that the repertoire of target gene differs from one
 tissue to another. In order to distinguish between the direct and indirect actions of TH in&amp;nbsp;vivo, we use the CRE/LoxP recombinati...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3097817</comments>
            <pubDate>Sat, 10 Jan 2009 11:03:22 +0100</pubDate>
            <guid isPermaLink="false">3097817</guid>        </item>
        <item>
            <title>Use of a new model of transgenic mice to clarify the respective functions of thyroid hormone receptors in vivo</title>
            <link>http://www.medworm.com/index.php?rid=2097622&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F503440v6k5645u61%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;3,5,3′-Triido-l-thyronine (T3) exerts pleiotropic actions on development and homeostasis mostly via its nuclear receptors, TRα1, TRβ1, and
 TRβ2, encoded by the THRA and THRB genes. Μouse genetics data outline the contrasting functions of THRA and THRB, and suggest
 that these are dictated by both the respective abundance of the receptor isoforms in a given cell type and the differences
 in the intrinsic properties of the receptors. The diversity of consequences of either hypothyroidism or THRA/THRB mutation
 is astonishing, suggesting that TR controls a large number of genes and that the repertoire of target gene differs from one
 tissue to another. In order to distinguish between the direct and indirect actions of TH in&amp;nbsp;vivo, we use the CRE/LoxP recombinati...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2097622</comments>
            <pubDate>Sat, 10 Jan 2009 11:03:22 +0100</pubDate>
            <guid isPermaLink="false">2097622</guid>        </item>
        <item>
            <title>Cardiac hypertrophy and thyroid hormone signaling</title>
            <link>http://www.medworm.com/index.php?rid=2086566&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F37668832840g6n81%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Thyroid hormone exerts a large number of influences on the cardiovascular system. Increased thyroid hormone action increases
 the force and speed of systolic contraction and the speed of diastolic relaxation and these are largely beneficial effects.
 Furthermore, thyroid hormone has marked electrophysiological effects increasing heart rate and the propensity for atrial fibrillation
 and these effects are largely mal-adaptive. In addition, thyroid hormone markedly increases cardiac angiogenesis and decreases
 vascular tone. These multiple thyroid hormone effects are largely mediated by the action of nuclear based thyroid hormone
 receptors (TR) the thyroid hormone receptor alpha and beta. TRα is the predominant isoform in the heart. Rapid nongenomic
 thyroid hormone eff...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2086566</comments>
            <pubDate>Tue, 06 Jan 2009 16:09:44 +0100</pubDate>
            <guid isPermaLink="false">2086566</guid>        </item>
        <item>
            <title>β-Adrenergic stimulation and myocardial function in the failing heart</title>
            <link>http://www.medworm.com/index.php?rid=2072959&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F8581121024985045%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The sympathetic nervous system provides the most powerful stimulation of cardiac function, brought about via norepinephrine
 and epinephrine and their postsynaptic β-adrenergic receptors. More than 30&amp;nbsp;years after the first use of practolol in patients
 with heart failure betablockers are now the mainstay of the pharmacological treatment of chronic heart failure. Many aspects
 of their mechanism of action are well understood, but others remain unresolved. This review focuses on a number of questions
 that are key to further developments in the field. What accounts for and what is the role of β-adrenergic desensitization,
 a hallmark of the failing heart? Is part of this adaptation predominantly beneficial and should therefore be reinforced, another
 part mainly ma...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2072959</comments>
            <pubDate>Sun, 28 Dec 2008 07:05:44 +0100</pubDate>
            <guid isPermaLink="false">2072959</guid>        </item>
        <item>
            <title>The role of thyroid hormone in the pathophysiology of heart failure: clinical evidence</title>
            <link>http://www.medworm.com/index.php?rid=2072960&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fm78379178q126762%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Thyroid hormone (TH) has a fundamental role in cardiovascular homeostasis in both physiological and pathological conditions,
 influencing cardiac contractility, heart rate (HR), diastolic function and systemic vascular resistance (SVR) through genomic
 and non-genomic mediated effects. In heart failure (HF) the main alteration of thyroid function is referred to as “low-triiodothyronine
 (T3) syndrome” (LT3S) characterized by decreased total serum T3 and free T3 (fT3) with normal levels of thyroxine (T4) and
 thyrotropin (TSH). Even if commonly interpreted as an adaptive factor, LT3S may have potential negative effects, contributing
 to the progressive deterioration of cardiac function and myocardial remodeling in HF and representing a powerful predictor
 of mortalit...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2072960</comments>
            <pubDate>Sun, 28 Dec 2008 07:05:41 +0100</pubDate>
            <guid isPermaLink="false">2072960</guid>        </item>
        <item>
            <title>Cardiomyocyte-specific inactivation of thyroid hormone in pathologic ventricular hypertrophy: an adaptative response or part of the problem?</title>
            <link>http://www.medworm.com/index.php?rid=2064908&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fq1t782kw12378071%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Recent studies in various rodent models of pathologic ventricular hypertrophy report the re-expression of deiodinase type
 3 (D3) in cardiomyocytes. D3 inactivates thyroid hormone (T3) and is mainly expressed in tissues during development. The stimulation
 of D3 activity in ventricular hypertrophy and subsequent heart failure is associated with severe impairment of cardiac T3
 signaling. Hypoxia-induced signaling appears to drive D3 expression in the hypertrophic cardiomyocyte, but other signaling
 cascades implicated in hypertrophy are also capable of stimulating transcription of the DIO3 gene. Many cardiac genes are transcriptionally regulated by T3 and impairment of T3 signaling will not only reduce energy
 turnover, but also lead to changes in gene expression that c...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2064908</comments>
            <pubDate>Wed, 24 Dec 2008 07:43:09 +0100</pubDate>
            <guid isPermaLink="false">2064908</guid>        </item>
        <item>
            <title>Relaxin, a pleiotropic vasodilator for the treatment of heart failure</title>
            <link>http://www.medworm.com/index.php?rid=2059663&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F586kj33348m11334%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Relaxin is a naturally occurring peptide hormone that plays a central role in the hemodynamic and renovascular adaptive changes
 that occur during pregnancy. Triggering similar changes could potentially be beneficial in the treatment of patients with
 heart failure. The effects of relaxin include the production of nitric oxide, inhibition of endothelin, inhibition of angiotensin
 II, production of VEGF, and production of matrix metalloproteinases. These effects lead to systemic and renal vasodilation,
 increased arterial compliance, and other vascular changes. The recognition of this has led to the study of relaxin for the
 treatment of heart failure. An initial pilot study has shown favorable hemodynamic effects in patients with heart failure,
 including reduction in v...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2059663</comments>
            <pubDate>Sun, 21 Dec 2008 08:37:09 +0100</pubDate>
            <guid isPermaLink="false">2059663</guid>        </item>
        <item>
            <title>Levosimendan: from basic science to clinical practice</title>
            <link>http://www.medworm.com/index.php?rid=2059664&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fv106w58n2655m431%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Levosimendan is a new cardiac enhancer that exerts positive inotropic effects on the failing heart mediated by calcium sensitization
 of contractile proteins as well as peripheral vasodilatory effects mediated by opening of ATP-sensitive potassium channels
 in vascular smooth-muscle cells. Levosimendan is the most well-studied calcium sensitizer in the real clinical practice, producing
 greater hemodynamic and symptomatic improvement in patients with acute heart failure syndromes (AHFS) than those with traditional
 inotropes. Immunomodulatory and anti-apoptotic properties of levosimendan may be an additional biologic mechanism that prevents
 further cytotoxic and hemodynamic consequences of abnormal immune and neurohormonal responses in AHFS. Recent mortality trials
 sh...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2059664</comments>
            <pubDate>Sun, 21 Dec 2008 08:37:06 +0100</pubDate>
            <guid isPermaLink="false">2059664</guid>        </item>
        <item>
            <title>The role of thyroid hormone nuclear receptors in the heart: evidence from pharmacological approaches</title>
            <link>http://www.medworm.com/index.php?rid=2055578&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F35845q193868766w%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;This review evaluates the hypothesis that the cardiac effects of amiodarone can be explained—at least partly—by the induction
 of a local ‘hypothyroid-like condition’ in the heart. Evidence supporting the hypothesis comprises the observation that amiodarone
 exerts an inhibitory effect on the binding of T3 to thyroid hormone receptors (TR) alpha-1 and beta-1 in&amp;nbsp;vitro, and on the
 expression of particular T3-dependent genes in&amp;nbsp;vivo. In the heart, amiodarone decreases heart rate and alpha myosin heavy
 chain expression (mediated via TR alpha-1), and increases sarcoplasmic reticulum calcium-activated ATPase and beta myosin
 heavy chain expression (mediated via TR beta-1). Recent data show a significant similarity in expression profiles of 8,435
 genes in ...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2055578</comments>
            <pubDate>Fri, 19 Dec 2008 08:24:35 +0100</pubDate>
            <guid isPermaLink="false">2055578</guid>        </item>
        <item>
            <title>Phosphodiesterase inhibition in heart failure</title>
            <link>http://www.medworm.com/index.php?rid=2055579&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ft08j651m41323863%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Drugs that inhibit cyclic nucleotide phosphodiesterase activity act to increase intracellular cyclic adenosine monophosphate
 (cAMP) and cyclic guanosine monophosphate (cGMP) content. In total, 11 families of these enzymes—which differ with respect
 to affinity for cAMP and cGMP, cellular expression, intracellular localization, and mechanisms of regulation—have been identified.
 Inhibitors of enzymes in the PDE3 family of cyclic nucleotide phosphodiesterases raise intracellular cAMP content in cardiac
 and vascular smooth muscle, with inotropic and, to a lesser extent, vasodilatory actions. These drugs have been used for many
 years in the treatment of patients with heart failure, but their long-term use has generally been shown to increase mortality
 through mechan...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2055579</comments>
            <pubDate>Fri, 19 Dec 2008 08:24:31 +0100</pubDate>
            <guid isPermaLink="false">2055579</guid>        </item>
        <item>
            <title>Vasodilators in the treatment of acute heart failure: what we know, what we don’t</title>
            <link>http://www.medworm.com/index.php?rid=2055580&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj28674045kx6k023%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Although we have recently witnessed substantial progress in management and outcome of patients with chronic heart failure,
 acute heart failure (AHF) management and outcome have not changed over almost a generation. Vasodilators are one of the cornerstones
 of AHF management; however, to a large extent, none of those currently used has been examined by large, placebo-controlled,
 non-hemodynamic monitored, prospective randomized studies powered to assess the effects on outcomes, in addition to symptoms.
 In this article, we will discuss the role of vasodilators in AHF trying to point out which are the potentially best indications
 to their administration and which are the pitfalls which may be associated with their use. Unfortunately, most of this discussion
 is only pa...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2055580</comments>
            <pubDate>Fri, 19 Dec 2008 08:24:27 +0100</pubDate>
            <guid isPermaLink="false">2055580</guid>        </item>
        <item>
            <title>An integrated approach to managing sleep disordered breathing and cardiovascular disease</title>
            <link>http://www.medworm.com/index.php?rid=2013214&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fu0632607rml8ngl3%2F</link>
            <description>This article
 will present a brief review of current processes used to diagnose and treat SDB, followed by a discussion of the overlap that
 exists between CVD and SDB, and present an argument that these chronic conditions should not be considered and managed as
 separate entities.
 
	Content Type Journal ArticleDOI 10.1007/s10741-008-9117-7Authors
		Robin J. Trupp, The Ohio State University College of Nursing Columbus OH USAElizabeth J. Corwin, The Ohio State University College of Nursing Columbus OH USA
	

	
		Journal Heart Failure ReviewsOnline ISSN 1573-7322Print ISSN 1382-4147 (Source: Heart Failure Reviews)</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2013214</comments>
            <pubDate>Wed, 03 Dec 2008 08:33:59 +0100</pubDate>
            <guid isPermaLink="false">2013214</guid>        </item>
        <item>
            <title>Biomarkers in heart failure: a clinical review</title>
            <link>http://www.medworm.com/index.php?rid=2013213&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fu44562167j725668%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The diagnosis and management of heart failure remains challenging despite considerable clinical advances in recent decades.
 With greater understanding of the pathophysiology of this complex syndrome, a large number of candidate biomarkers have emerged
 and duly received scientific and clinical attention. These are frequently a measure of the degree of pathophysiological derangement
 or counter-regulatory processes occurring in heart failure and include biomarkers of neurohormonal activation, myocyte necrosis
 and myocardial remodelling amongst others. As such they may serve as an indicator of the presence, severity and possibly therapeutic
 response of the heart failure syndrome and may complement conventional clinical measurements and acumen. This may in turn
 lead to...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2013213</comments>
            <pubDate>Wed, 03 Dec 2008 08:33:59 +0100</pubDate>
            <guid isPermaLink="false">2013213</guid>        </item>
        <item>
            <title>Sleep-associated movement disorders and heart failure</title>
            <link>http://www.medworm.com/index.php?rid=2013212&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc768802445116710%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Sleep-associated movement disorders are a broad group of sleep disorders characterized by involuntary movements that may disrupt
 sleep. Relatively little is known about the clinical consequences of sleep-associated movement disorders on cardiovascular
 health. Because these disorders manifest mostly during sleep, recognizing a movement disorder can be particularly difficult.
 Nevertheless, patients can have frequent arousals and suffer from similar sleep deprivation, fragmentation, and autonomic
 disruption as occurs in sleep-disordered breathing. Subsequently, these disorders may have a serious impact on daytime function
 and perception of health in patients with chronic heart failure.
 
	Content Type Journal ArticleDOI 10.1007/s10741-008-9118-6Authors
		Troy Schaffer...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2013212</comments>
            <pubDate>Wed, 03 Dec 2008 08:33:59 +0100</pubDate>
            <guid isPermaLink="false">2013212</guid>        </item>
        <item>
            <title>Cardiac effects of thyronamines</title>
            <link>http://www.medworm.com/index.php?rid=1974415&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ftr4t005h5k7v7144%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;3-Iodothyronamine (T1AM) is an endogenous compound derived from thyroid hormone through decarboxylation and deiodination, which interacts with
 a novel G protein-coupled receptor, known as trace amine-associated receptor 1 (TAAR1). TAAR1 and other receptors of this
 family are expressed in several tissues, including the heart. Functional effects have been observed after administration of
 exogenous T1AM: in the isolated heart, a negative inotropic and chronotropic action was produced, and the resistance to ischemic injury
 was increased, possibly as a consequence of an action on intracellular calcium homeostasis. Extracardiac effects include reduction
 of body temperature, increased lipid versus carbohydrate metabolism, and modulation of insulin secretion. T1AM might pl...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1974415</comments>
            <pubDate>Wed, 19 Nov 2008 19:03:25 +0100</pubDate>
            <guid isPermaLink="false">1974415</guid>        </item>
        <item>
            <title>Physiological consequences of the TRα1 aporeceptor state</title>
            <link>http://www.medworm.com/index.php?rid=1963624&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F3472776215k5l170%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Many patients have been characterized harboring a mutation in thyroid hormone receptor (TR) β. Surprisingly none has yet been
 identified carrying a mutation in TRα1. To facilitate the identification of such patients, several animal models with a mutant
 TRα1 have been generated. While some phenotypic characteristics, such as an adult euthyroidism, are similar in the mutant
 mice, other aspects such as metabolism are quite variable. This review summarizes the most important consequences of a mutation
 in TRα1 in mice focusing on the TRα1-R384C mutation, and projects the insights from the animal models to a putative phenotype
 of patients with a mutated TRα1.
 
	Content Type Journal ArticleDOI 10.1007/s10741-008-9119-5Authors
		Jens Mittag, Karolinska Institute Dep...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1963624</comments>
            <pubDate>Fri, 14 Nov 2008 08:06:15 +0100</pubDate>
            <guid isPermaLink="false">1963624</guid>        </item>
        <item>
            <title>Sobetirome: a case history of bench-to-clinic drug discovery and development</title>
            <link>http://www.medworm.com/index.php?rid=1954862&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fp573462351260p74%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Sobetirome, also known as GC-1 and QRX-431, is a member of a class of compounds known as selective thyromimetics (Scanlan
 et al., Curr Opin Drug Discov Dev 4:614–622). These compounds are synthetic structural analogs of thyroid hormone that have
 tissue-specific thyroid hormone actions. Many of the compounds in this class, including sobetirome, also are subtype-selective
 thyroid hormone receptor (TR) agonists. Sobetirome selectively binds to and activates TRβ over TRα and this receptor selectivity
 led to the hypothesis that sobetirome would lower cholesterol through activation of liver TRβ without stimulating cardiac
 function through TRα activation in the heart. The tissue selective thyromimetic properties of sobetirome have been demonstrated
 in numerous anim...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1954862</comments>
            <pubDate>Tue, 11 Nov 2008 08:01:33 +0100</pubDate>
            <guid isPermaLink="false">1954862</guid>        </item>
        <item>
            <title>PPAR transcriptional activator complex polymorphisms and the promise of individualized therapy for heart failure</title>
            <link>http://www.medworm.com/index.php?rid=1946611&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh2374210293r337k%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The PPAR gene pathway consists of interrelated genes that encode transcription factors, enzymes, and downstream targets which
 coordinately act to regulate cellular processes central to glucose and lipid metabolism. The pathway includes the PPAR genes
 themselves, other class II nuclear hormone receptor transcription factors within the PPAR family, PPAR co-activators, PPAR
 co-repressors, and downstream metabolic gene targets. This review focuses on the transcription factors that comprise the PPAR
 transcriptional activator complex—the PPARs (PPARα, PPARβ, or PPARγ), PPAR heterodimeric partners, such as RXRα, and PPAR
 co-activators, such as PPARγ coactivator 1α (PGC-1α) and the estrogen-related receptors (ERRα, ERRβ, and ERRγ). These transcription
 factors ...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1946611</comments>
            <pubDate>Sun, 09 Nov 2008 10:08:55 +0100</pubDate>
            <guid isPermaLink="false">1946611</guid>        </item>
        <item>
            <title>Understanding the pharmacogenetic approach to warfarin dosing</title>
            <link>http://www.medworm.com/index.php?rid=1946612&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F11pn670222271637%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Warfarin remains the drug of choice for long-term anticoagulation management in a variety of conditions. Despite an established
 role in prevention of thromboembolic events such as stroke, warfarin continues to be underutilized because of its association
 with serious drug-related adverse events. Lacking alternative therapeutic approaches, intensive research in the past decade
 has focused on making anticoagulation with warfarin safer. Much emphasis has been placed on defining factors associated with
 the wide individual variability in warfarin dose. Polymorphic sites in three genes, cytochrome P450 (CYP) 2C9, vitamin K 2,3
 epoxide reductase complex 1 (VKORC1), and CYP4F2, have been shown to affect stable warfarin dose. An overview of the persistent
 issues related to ...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1946612</comments>
            <pubDate>Sun, 09 Nov 2008 10:08:54 +0100</pubDate>
            <guid isPermaLink="false">1946612</guid>        </item>
        <item>
            <title>Introduction: vasopressin therapy</title>
            <link>http://www.medworm.com/index.php?rid=1944949&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F321124h732g20064%2F</link>
            <description>Content Type Journal ArticleDOI 10.1007/s10741-008-9116-8Authors
		David J. Whellan, Jefferson Medical College Department of Medicine, Division of Cardiology Philadelphia PA 19017 USA
	

	
		Journal Heart Failure ReviewsOnline ISSN 1573-7322Print ISSN 1382-4147 (Source: Heart Failure Reviews)</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1944949</comments>
            <pubDate>Fri, 07 Nov 2008 08:20:17 +0100</pubDate>
            <guid isPermaLink="false">1944949</guid>        </item>
        <item>
            <title>Genetic variation in the natriuretic peptide system and heart failure</title>
            <link>http://www.medworm.com/index.php?rid=1875585&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj57822626t713322%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Heart failure (HF) is a modern epidemic and is one of the few cardiovascular diseases which is increasing in prevalence. The
 growing importance of the Natriuretic Peptide (NP) system in HF is well recognized. Laboratory tests for B-type Natriuretic
 Peptide (BNP) have proven value as diagnostic and prognostic tools in HF and are now part of routine clinical care. Furthermore,
 recombinant atrial natriuretic peptide (ANP) (carperitide) and BNP (nesiritide) and are approved HF therapies in Japan and
 the US, respectively and additional natriuretic peptides (e.g., CNP, urodilatin, and designer NPs) are under investigation
 for use in HF. Common genetic sequence variants are increasingly being recognized as determinants of disease risk or drug
 response and may help explai...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1875585</comments>
            <pubDate>Sat, 11 Oct 2008 11:27:42 +0100</pubDate>
            <guid isPermaLink="false">1875585</guid>        </item>
        <item>
            <title>Obstructive sleep apnea: the new cardiovascular disease. Part I: obstructive sleep apnea and the pathogenesis of vascular disease</title>
            <link>http://www.medworm.com/index.php?rid=1814964&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fy34t0518661428q0%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Obstructive sleep apnea (OSA) is increasingly recognized as a novel cardiovascular risk factor. OSA is implicated in the pathogenesis
 of hypertension, left ventricular dysfunction, coronary artery disease and stroke. OSA exerts its negative cardiovascular
 consequences through its unique pattern of intermittent hypoxia. Endothelial dysfunction, oxidative stress, and inflammation
 are all consequences of OSA directly linked to intermittent hypoxia and critical pathways in the pathogenesis of cardiovascular
 disease in patients with OSA. This review will discuss the known mechanisms of vascular dysfunction in patients with OSA and
 their implications for cardiovascular disease.
 
	Content Type Journal ArticleDOI 10.1007/s10741-008-9112-zAuthors
		Rami Khayat, The Ohio St...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1814964</comments>
            <pubDate>Sat, 20 Sep 2008 10:16:57 +0100</pubDate>
            <guid isPermaLink="false">1814964</guid>        </item>
        <item>
            <title>Treatment options for hyponatremia in heart failure</title>
            <link>http://www.medworm.com/index.php?rid=1782104&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fn248p1742j32l5k0%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Hyponatremia is independently associated with adverse outcomes in patients with congestive heart failure (CHF). The primary
 cause of hyponatremia in CHF is the inappropriate secretion of the antidiuretic hormone, arginine vasopressin (AVP). The binding
 of AVP to V2 receptors in the renal collecting duct promotes water retention, a process that can lead to dilutional hyponatremia as well
 as increased ventricular preload. AVP could also exacerbate the course of CHF by interacting with V1A receptors on vascular smooth muscle cells and myocytes. Conventional treatment of hyponatremia in CHF is based largely on
 water restriction, which is neither effective nor well tolerated. Current research is exploring V2- and dual V1A/V2-receptor antagonism for the treatment of hypon...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1782104</comments>
            <pubDate>Tue, 09 Sep 2008 00:21:07 +0100</pubDate>
            <guid isPermaLink="false">1782104</guid>        </item>
        <item>
            <title>Rebuilding the post-infarcted myocardium by activating ‘physiologic’ hypertrophic signaling pathways: the thyroid hormone paradigm</title>
            <link>http://www.medworm.com/index.php?rid=1775021&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F148445g2hv141195%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Viable myocardium undergoes several changes in the course of cardiac remodeling following myocardial infarction aiming to
 adapt the heart to the hemodynamic compromise. This response is characterized by reactivation of the fetal transcriptional
 program and results in cardiac dysfunction. Changes in thyroid hormone (TH)-TH receptors (TRs) axis occur in the course of
 post-infarction cardiac remodeling and seem to contribute to cardiac fetal phenotype. TH can “rebuild” the post-infarcted
 heart by preventing the fetal-like pattern of contractile proteins expression, normalizing wall tension, and optimizing cardiac
 chamber geometry. This effect seems to be attributed to TH pleiotropic cellular actions; TH promotes tissue growth and differentiation
 and favorably rem...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1775021</comments>
            <pubDate>Fri, 05 Sep 2008 17:50:35 +0100</pubDate>
            <guid isPermaLink="false">1775021</guid>        </item>
        <item>
            <title>AVP receptor antagonists in patients with CHF</title>
            <link>http://www.medworm.com/index.php?rid=1763498&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh42386k06h2t226v%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;In the Adhere (Acute Decompensated Heart Failure Registry) National Registry, hyponatremia (serum sodium&amp;nbsp;&amp;lt;130&amp;nbsp;mEq/l) at clinical
 presentation was noted in 5% of patients with HF. The enhanced release of arginine vasopressin (AVP) can lead to hyponatremia
 by binding to the V2 receptor results in free-water retention and hyponatremia. Given the central role of AVP in causing hyponatremia
 in patients with congestive heart failure, decreasing vasopressin activity has been a therapeutic focus. With no current therapy
 to decrease production of AVP, attention was turned to decreasing the effect of AVP by blocking the receptor.
 
	Content Type Journal ArticleDOI 10.1007/s10741-008-9107-9Authors
		Siva K. Kumar, Jefferson Medical College Thomas Jefferson Univers...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1763498</comments>
            <pubDate>Wed, 03 Sep 2008 08:45:19 +0100</pubDate>
            <guid isPermaLink="false">1763498</guid>        </item>
        <item>
            <title>Pharmacology of vasopressin antagonists</title>
            <link>http://www.medworm.com/index.php?rid=1763497&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F237538r375r5w186%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Congestive heart failure (CHF) is characterized by fluid and water retention, which frequently is a therapeutic challenge.
 Most conventional diuretics act primarily as saluretics, i.e. they inhibit renal tubular electrolyte reabsorption, which due
 to osmotic pressure promotes excretion of isotonic fluid. Arginine vasopressin (AVP) via the V1A receptor vasoconstricts and via the V2 receptor promotes water reabsorption in the renal collecting duct by inserting aquaporin-2 water channels into the luminal
 membrane. Novel V2 receptor antagonists act as powerful aquaretics, i.e. they excrete free water. We review the pharmacology of non-selective
 V1A/V2 receptor antagonists and selective V2 receptor antagonists currently in clinical development.
 
	Content Type Journal Ar...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1763497</comments>
            <pubDate>Wed, 03 Sep 2008 08:45:19 +0100</pubDate>
            <guid isPermaLink="false">1763497</guid>        </item>
        <item>
            <title>Insomnia and chronic heart failure</title>
            <link>http://www.medworm.com/index.php?rid=1749784&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fy5h54811276n7v22%2F</link>
            <description>This article reviews insomnia in CHF, cardiac medication side-effects
 related to sleep disturbances, and treatment options.
 
	Content Type Journal ArticleDOI 10.1007/s10741-008-9102-1Authors
		Don Hayes, University of Kentucky College of Medicine J410 Kentucky Clinic Departments of Pediatrics and Internal Medicine 740 South Limestone Street Lexington KY 40536 USAMichael I. Anstead, University of Kentucky College of Medicine J410 Kentucky Clinic Departments of Pediatrics and Internal Medicine 740 South Limestone Street Lexington KY 40536 USAJulia Ho, University of Kentucky HealthCare Department of Pharmacy 800 Rose Street H-110 Lexington KY 40536-0293 USABarbara A. Phillips, University of Kentucky, Samaritan Sleep Center Department of Internal Medicine 310 South Limestone Street Lexington...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1749784</comments>
            <pubDate>Sat, 30 Aug 2008 11:03:23 +0100</pubDate>
            <guid isPermaLink="false">1749784</guid>        </item>
        <item>
            <title>Hyponatremia in heart failure concluding remarks</title>
            <link>http://www.medworm.com/index.php?rid=1749787&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fe03m1045q313u675%2F</link>
            <description>Content Type Journal ArticleDOI 10.1007/s10741-008-9106-xAuthors
		Kanu Chatterjee, UCSF Norwich CT USA
	

	
		Journal Heart Failure ReviewsOnline ISSN 1573-7322Print ISSN 1382-4147 (Source: Heart Failure Reviews)</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1749787</comments>
            <pubDate>Sat, 30 Aug 2008 11:03:22 +0100</pubDate>
            <guid isPermaLink="false">1749787</guid>        </item>
        <item>
            <title>Hyponatremia in heart failure</title>
            <link>http://www.medworm.com/index.php?rid=1749786&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fn68u64612n8w9782%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Hyponatremia is the most common electrolyte abnormality found in hospitalized patients with heart failure. It may occur in
 patients who have hypovolemic, hypervolemic, or euvolemic state. It is usually not corrected by available therapies. It is
 a major predictor of prognosis, and correction of hyponatremia can be effectively accomplished by vasopressin antagonists.
 However, it still remains to be seen whether the normalization of serum sodium with vasopressin antagonists will also lead
 to an improved long-term prognosis.
 
	Content Type Journal ArticleDOI 10.1007/s10741-008-9109-7Authors
		Dimitrios Farmakis, Attikon University Hospital Second Department of Cardiology, Heart Failure Unit Athens GreeceGerasimos Filippatos, Attikon University Hospital Second Departme...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1749786</comments>
            <pubDate>Sat, 30 Aug 2008 11:03:22 +0100</pubDate>
            <guid isPermaLink="false">1749786</guid>        </item>
        <item>
            <title>OSA: the new cardiovascular disease</title>
            <link>http://www.medworm.com/index.php?rid=1749785&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ff566165v44221683%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Obstructive sleep apnea (OSA), present in 5–15% of adults, is strongly associated with the incidence and poor outcome of hypertension,
 coronary artery disease, arrhythmia, heart failure, and stroke. Treatment of OSA completely reverses its cardiovascular consequences.
 In this review, we discuss the clinical evidence for the strong association between OSA and cardiovascular disease and present
 an argument for approaching OSA as a cardiovascular disease. We particularly focus on the causative relationship between OSA
 and hypertension, and on the increasingly recognized relationship between OSA and heart failure.
 
	Content Type Journal ArticleDOI 10.1007/s10741-008-9101-2Authors
		Kiran Devulapally, Ohio State University Division of Pulmonary, Critical Care, and Sle...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1749785</comments>
            <pubDate>Sat, 30 Aug 2008 11:03:22 +0100</pubDate>
            <guid isPermaLink="false">1749785</guid>        </item>
        <item>
            <title>Central sleep apnea in patients with congestive heart failure</title>
            <link>http://www.medworm.com/index.php?rid=1749789&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F5r433w2720361571%2F</link>
            <description>This article will review the determinants
 of central apnea, the specific features of CHF-related central apnea, and outline a management approach
 
	Content Type Journal ArticleCategory Apnea in Heart FailureDOI 10.1007/s10741-008-9100-3Authors
		Safwan Badr, Wayne State University Detroit USA
	

	
		Journal Heart Failure ReviewsOnline ISSN 1573-7322Print ISSN 1382-4147 (Source: Heart Failure Reviews)</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1749789</comments>
            <pubDate>Sat, 30 Aug 2008 11:03:21 +0100</pubDate>
            <guid isPermaLink="false">1749789</guid>        </item>
        <item>
            <title>Diastolic dysfunction in exercise and its role for exercise capacity</title>
            <link>http://www.medworm.com/index.php?rid=1749788&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fm001661r70p26888%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Diastolic dysfunction is frequent in elderly subjects and in patients with left ventricular hypertrophy, vascular disease
 and diabetes mellitus. Patients with diastolic dysfunction demonstrate a reduced exercise capacity and might suffer from congestive
 heart failure (CHF). Presence of symptoms of CHF in the setting of a normal systolic function is referred to as heart failure
 with normal ejection fraction (HFNEF) or, if evidence of an impaired diastolic function is observed, as diastolic heart failure
 (DHF). Reduced exercise capacity in diastolic dysfunction results from a number of pathophysiological alterations such as
 slowed myocardial relaxation, reduced myocardial distensibility, elevated filling pressures, and reduced ventricular suction
 forces. These alter...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1749788</comments>
            <pubDate>Sat, 30 Aug 2008 11:03:21 +0100</pubDate>
            <guid isPermaLink="false">1749788</guid>        </item>
        <item>
            <title>Sleep-disordered breathing in patients with decompensated heart failure</title>
            <link>http://www.medworm.com/index.php?rid=1749790&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fv7p773024110t191%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Sleep-disordered breathing (SDB) has a higher prevalence in patients with heart failure than in the general middle-aged population.
 Obstructive sleep apnea (OSA), one of the forms of SBD, promotes poorly controlled hypertension, coronary events, and atrial
 fibrillation events that can lead to acutely decompensated heart failure (ADHF), and evidence suggests that untreated OSA
 increases mortality in patients with heart failure. Cheyne–Stokes respiration and central sleep apnea (CSA) have long been
 associated with heart failure and, in many patients, can coexist with OSA. In this article, we propose a systematic approach
 to diagnose and treat OSA in patients with ADHF based on current evidence.
 
	Content Type Journal ArticleDOI 10.1007/s10741-008-9103-0Authors
		M...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1749790</comments>
            <pubDate>Sat, 30 Aug 2008 11:03:20 +0100</pubDate>
            <guid isPermaLink="false">1749790</guid>        </item>
        <item>
            <title>Biology of TNFα and IL-10, and their imbalance in heart failure</title>
            <link>http://www.medworm.com/index.php?rid=1723017&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx1088u466l355254%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Our understanding of the multiple in vivo functions of the proinflammatory cytokine, tumor necrosis factor (TNFα), is advancing
 at a rapid pace. In addition to its antitumor effects, overproduction of TNFα provokes tissue injury and organ failure. TNFα
 has also been shown to be cardiodepressent and responsible for various cardiovascular complications. It appears that still
 much needs to be learned for a full comprehension of the role of TNFα in heart biology. Another cytokine, interleukin-10 (IL-10),
 has been shown to have anti-inflammatory properties. It is suggested to counterbalance many adverse effects of TNFα. IL-10
 suppresses the production of TNFα and many other proinflammatory cytokines. TNFα-induced oxidative stress is also known to
 be mitigated by...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1723017</comments>
            <pubDate>Tue, 19 Aug 2008 17:24:52 +0100</pubDate>
            <guid isPermaLink="false">1723017</guid>        </item>
        <item>
            <title>Treatment of sleep disordered breathing in congestive heart failure</title>
            <link>http://www.medworm.com/index.php?rid=1615225&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj7t3337081204113%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;In patients with congestive heart failure, sleep disordered breathing occurs commonly and is associated with an increased
 mortality. In addition to central sleep apnea (Cheyne–Stokes respiration), obstructive sleep apnea is more prevalent in patients
 with congestive heart failure than in the general population. As a result, a number of treatments have been investigated,
 with varying results. While many therapies may improve the severity of sleep disordered breathing, only positive pressure
 ventilation has been shown to improve cardiac function. Newer forms of positive pressure ventilation, such as adaptive servo-ventilation,
 appear to be even more effective at correcting central sleep apnea. Whether any of these treatments have an effect on transplant-free
 survi...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1615225</comments>
            <pubDate>Fri, 11 Jul 2008 07:25:43 +0100</pubDate>
            <guid isPermaLink="false">1615225</guid>        </item>
        <item>
            <title>Sleep disordered breathing in chronic heart failure</title>
            <link>http://www.medworm.com/index.php?rid=1518070&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F038037u761257l08%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Heart failure is a growing problem, placing an increasing burden on public health resources and continuing to exert a high
 toll in mortality and morbidity. Sleep disordered breathing (SDB) is also a major public health problem and is associated
 with an increased risk of fatal and non-fatal cardiovascular events. Current evidence suggests SDB, particularly central SDB,
 is more prevalent in patients with chronic heart failure (CHF) than in the general population, but is under-diagnosed as SDB
 symptoms are less prevalent in CHF. This is further hampered by the absence of a simple and accurate screening tool and limited
 access to sleep facilities to diagnose SDB in the large numbers of patients with CHF. The presence of SDB in patients with
 CHF imposes increased haemo...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1518070</comments>
            <pubDate>Thu, 12 Jun 2008 06:28:30 +0100</pubDate>
            <guid isPermaLink="false">1518070</guid>        </item>
        <item>
            <title>Mechanical circulatory support devices for acute heart failure syndromes: considerations for clinical trial design</title>
            <link>http://www.medworm.com/index.php?rid=1518071&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fy7720261812u08w2%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Mechanical circulatory support (MCS) devices are a guideline-recommended treatment option for a small subset of advanced heart
 failure patients. MCS has the potential to become more prominent in the management of Acute Heart Failure Syndromes (AHFS)
 as device technology advances and as clinical trials consistently discover neutral or harmful effects with pharmacologic therapies
 hypothesized to be beneficial in this population. While it is now possible to identify AHFS patients who are at high risk
 of death, the therapeutic options available to improve their long-term outcomes are limited. MCS therapy in this population
 offers a “bridge to recovery” strategy; these patients may have viable myocardium that responds favorably to the influence
 of MCS on neurohormo...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1518071</comments>
            <pubDate>Thu, 12 Jun 2008 06:28:28 +0100</pubDate>
            <guid isPermaLink="false">1518071</guid>        </item>
        <item>
            <title>Genomics, heart failure and sudden cardiac death</title>
            <link>http://www.medworm.com/index.php?rid=1401973&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fl73325vm14736210%2F</link>
            <description>This article discusses the prospect of genomic science as an
 approach to the identification of patients at high-risk for SCD. While the final common pathway for SCD is malignant ventricular
 arrhythmias, there are many potential contributors, pathways, and mechanisms by which common genetic variants (polymorphisms)
 could affect initiation and propagation of life-threatening cardiac arrhythmias. Recent advances in genomic medicine now provide
 us with novel approaches to both identify candidate genes/pathways and relatively common polymorphisms which may predispose
 patients to increased risk for SCD. Improved understanding of the relationship between common polymorphisms and SCD will not
 only improve risk stratification such that ICDs can be targeted to those patients most likely to ben...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1401973</comments>
            <pubDate>Fri, 25 Apr 2008 10:18:03 +0100</pubDate>
            <guid isPermaLink="false">1401973</guid>        </item>
        <item>
            <title>β-Blocker pharmacogenetics in heart failure</title>
            <link>http://www.medworm.com/index.php?rid=1401974&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc4710p0507m67734%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;β-Blockers (metoprolol, bisoprolol, and carvedilol) are a cornerstone of heart failure (HF) treatment. However, it is well
 recognized that responses to a β-blocker are variable among patients with HF. Numerous studies now suggest that genetic polymorphisms
 may contribute to variability in responses to a β-blocker, including left ventricular ejection fraction improvement, survival,
 and hospitalization due to HF exacerbation. This review summarizes the pharmacogenetic data for β-blockers in patients with
 HF and discusses the potential implications of β-blocker pharmacogenetics for HF patients.
 
	Content Type Journal ArticleDOI 10.1007/s10741-008-9094-xAuthors
		Jaekyu Shin, University of Florida Department of Pharmacy Practice, College of Pharmacy, Center for Ph...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1401974</comments>
            <pubDate>Fri, 25 Apr 2008 10:18:00 +0100</pubDate>
            <guid isPermaLink="false">1401974</guid>        </item>
        <item>
            <title>Anemia treatment in chronic kidney disease: shifting uncertainty</title>
            <link>http://www.medworm.com/index.php?rid=1366456&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fpg4166420t386548%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Epidemiologic observations showing associations between higher levels of some biologic markers such as blood pressure and
 serum cholesterol with heightened risk of death and non-fatal cardiovascular events have provided important data to develop
 hypotheses regarding pharmacologic therapies to modify these markers to improve prognosis. Randomized controlled trials have
 shown that strategies to reduce blood pressure with a variety of antihypertensive agents and LDL cholesterol with statins
 do, indeed, result in important improvements in clinical outcomes. However, there are several instances where a hypothesis
 based on strong observational data has been rejected based on surprising counterintuitive evidence generated from randomized
 controlled clinical trials. Use o...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1366456</comments>
            <pubDate>Thu, 10 Apr 2008 07:06:06 +0100</pubDate>
            <guid isPermaLink="false">1366456</guid>        </item>
        <item>
            <title>Approaches to the treatment of anaemia in patients with chronic heart failure</title>
            <link>http://www.medworm.com/index.php?rid=1362244&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc8273377823p70k4%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;An association between anaemia, poor functional status and, compared to non-anaemic patients, worse clinical status and a
 higher risk of hospitalisation and death has been consistently reported in chronic heart failure (CHF), although cause an
 effect has not been proven. While it is attractive to think that correction of a co-morbidity that exacerbates already diminished
 delivery of oxygen to the tissues in heart failure is likely to beneficial, the possible haemodynamic effects of increasing
 haemoglobin, for example vasoconstriction, might not be. Consequently, the balance of benefit and risk of anaemia correction
 in CHF is uncertain, may vary according to the severity of anaemia (and other factors) and needs to be properly evaluated.
 To date, most studies of ana...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1362244</comments>
            <pubDate>Tue, 08 Apr 2008 07:19:46 +0100</pubDate>
            <guid isPermaLink="false">1362244</guid>        </item>
        <item>
            <title>Introduction: anemia in heart failure</title>
            <link>http://www.medworm.com/index.php?rid=1339952&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fq021083q50520j10%2F</link>
            <description>Content Type Journal ArticleDOI 10.1007/s10741-008-9093-yAuthors
		Inder Anand, University of Minnesota Medical School Minneapolis MN 55417 USA
	

	
		Journal Heart Failure ReviewsOnline ISSN 1573-7322Print ISSN 1382-4147 (Source: Heart Failure Reviews)</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1339952</comments>
            <pubDate>Sat, 29 Mar 2008 09:00:27 +0100</pubDate>
            <guid isPermaLink="false">1339952</guid>        </item>
        <item>
            <title>Role of central and peripheral aminopeptidase activities in the control of blood pressure: a working hypothesis</title>
            <link>http://www.medworm.com/index.php?rid=1339953&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fg6w03234706m4066%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Although there is a large body of knowledge on protein synthesis, the available data on protein catabolism, although quite
 substantial, are still inadequate. This is due to the marked differences in the activity of proteolytic enzymes, compounded
 by different substrate specificities and multiple environmental factors. Understanding enzyme behavior under physiological
 and pathological conditions requires the identification of specific proteolytic activities, such as aminopeptidases, as able
 to degrade certain peptidergic hormones or neuropeptides. Another requirement is the isolation, purification and characterization
 of the enzymes involved. In addition, systematic studies are needed to determine each enzyme’s subcellular location, tissue
 distribution, and the i...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1339953</comments>
            <pubDate>Sat, 29 Mar 2008 09:00:26 +0100</pubDate>
            <guid isPermaLink="false">1339953</guid>        </item>
        <item>
            <title>Psychobiology of depression/distress in congestive heart failure</title>
            <link>http://www.medworm.com/index.php?rid=1334351&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx2064l57v560u630%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Heart failure affects millions of Americans and new diagnosis rates are expected to almost triple over the next 30&amp;nbsp;years as
 our population ages. Affective disorders including clinical depression and anxiety are common in patients with congestive
 heart failure. Furthermore, the presence of these disorders significantly impacts quality of life, medical outcomes, and healthcare
 service utilization. In recent years, the literature has attempted to describe potential pathophysiologic mechanisms relating
 affective disorders and psychosocial stress to heart failure. Several potential mechanisms have been proposed including autonomic
 nervous system dysfunction, inflammation, cardiac arrhythmias, and altered platelet function. These mechanisms are reviewed
 in this art...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1334351</comments>
            <pubDate>Thu, 27 Mar 2008 18:38:35 +0100</pubDate>
            <guid isPermaLink="false">1334351</guid>        </item>
        <item>
            <title>Iron and anemia in human biology: a review of mechanisms</title>
            <link>http://www.medworm.com/index.php?rid=1328742&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh566428607070279%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The biology of iron in relation to anemia is best understood by a review of the iron cycle, since the majority of iron for
 erythropoiesis is provided by iron recovered from senescent erythrocytes. In iron-deficiency anemia, storage iron declines
 until iron delivery to the bone marrow is insufficient for erythropoiesis. This can be monitored with clinical indicators,
 beginning with low plasma ferritin, followed by decreased plasma iron and transferrin saturation, and culminating in red blood
 cells with low-Hb content. When adequate dietary iron is provided, these markers show return to normal, indicating a response
 to the dietary supplement. Anemia of inflammation (also known as anemia of chronic disease, or ACD) follows a different course,
 because in this form of ...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1328742</comments>
            <pubDate>Tue, 25 Mar 2008 07:12:39 +0100</pubDate>
            <guid isPermaLink="false">1328742</guid>        </item>
        <item>
            <title>Renin–angiotensin–aldosterone system (RAAS) pharmacogenomics: implications in heart failure management</title>
            <link>http://www.medworm.com/index.php?rid=1319017&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F600936534261g0m1%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Blockade of the renin–angiotensin–aldosterone system (RAAS) with ACE inhibitors has been a cornerstone of heart failure therapy
 for over 15&amp;nbsp;years. More recently, further blockade of RAAS with aldosterone antagonists and angiotensin receptor blockers
 (ARBs) has been studied. While these therapies have certainly improved outcomes in the treatment of heart failure, morbidity
 and mortality remain extremely high. Furthermore, polypharmacy and complex regimens of seven medications on average is the
 norm for management of heart failure. This results in increased costs, patient burden, and uncertainty as to the best course
 of therapy. The ability to personalize patients’ therapeutic regimens using pharmacogenomics has the potential of providing
 more effective a...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1319017</comments>
            <pubDate>Thu, 20 Mar 2008 09:33:13 +0100</pubDate>
            <guid isPermaLink="false">1319017</guid>        </item>
        <item>
            <title>Intracellular devastation in heart failure</title>
            <link>http://www.medworm.com/index.php?rid=1313879&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc31221q8142mh82k%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;End-stage heart failure is characterized by a number of abnormalities at the cellular level, which include changes in excitation–contraction
 coupling, alterations in contractile proteins and activation/deactivation of signaling pathways. Even though many of these
 changes are adaptive to the high workload and stress in heart failure, a significant number of these alterations are deeply
 deleterious to the cardiac cell. In this article, we will review the changes in calcium cycling that occur in myopathic hearts
 and how they can be effectively targeted. We will also focus on protein misfolding in the setting of cardiac dysfunction.
 
	Content Type Journal ArticleDOI 10.1007/s10741-007-9071-9Authors
		Federica del Monte, Beth Israel Deaconess Medical Center Cardiovasc...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1313879</comments>
            <pubDate>Tue, 18 Mar 2008 07:58:45 +0100</pubDate>
            <guid isPermaLink="false">1313879</guid>        </item>
        <item>
            <title>Pleiotropic effects of cardiac drugs on healing post-MI. The good, bad, and ugly</title>
            <link>http://www.medworm.com/index.php?rid=1217729&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fk0317858r56v0504%2F</link>
            <description>This article reviews the potential impact of pleiotropic effects of
 some prototypic cardiac drugs such as renin-angiotensin-aldosterone system (RAAS) inhibitors, statins, and thrombolytics during
 healing post-ST-segment-elevation MI (STEMI), with special focus on inflammation, ECCM and remodeling, and implications in
 the elderly.
 
	Content Type Journal ArticleDOI 10.1007/s10741-008-9090-1Authors
		Bodh I. Jugdutt, University of Alberta Division of Cardiology, Department of Medicine and Cardiovascular Research Group, Faculty of Medicine Edmonton Canada
	

	
		Journal Heart Failure ReviewsOnline ISSN 1573-7322Print ISSN 1382-4147 (Source: Heart Failure Reviews)</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1217729</comments>
            <pubDate>Thu, 07 Feb 2008 18:17:13 +0100</pubDate>
            <guid isPermaLink="false">1217729</guid>        </item>
        <item>
            <title>The prevalence of anemia in chronic heart failure and its impact on the clinical outcomes</title>
            <link>http://www.medworm.com/index.php?rid=1197910&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F67088u8309401873%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;This review article summarizes the current medical literature reporting on the prevalence and prognostic significance of anemia
 in patients with heart failure. Almost all currently available data indicate that anemia is common in heart failure populations,
 with the majority of studies indicating prevalence &amp;gt;20%. Anemia appears to be more highly prevalent in patients with advanced
 age, with more severe limitations in functional capacity, and with greater severity of co-morbid chronic kidney disease. In
 most reported studies anemia is an independent predictor of increased mortality risk and increased risk of hospitalization
 for heart failure. These data provide the rationale for interventional treatment trials to determine if anemia is in the causal
 pathway for d...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1197910</comments>
            <pubDate>Sat, 02 Feb 2008 16:50:07 +0100</pubDate>
            <guid isPermaLink="false">1197910</guid>        </item>
        <item>
            <title>Heart failure and anemia: mechanisms and pathophysiology</title>
            <link>http://www.medworm.com/index.php?rid=1195770&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ff1567xr04669167r%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Anemia is a common comorbidity in patients with heart failure and affects up to 50% of patients, depending on the definition
 of anemia used and on the population studied. Presence of anemia and lower hemoglobin (Hgb) concentrations are powerful independent
 predictors of adverse outcomes in heart failure. Even small reductions in Hgb are associated with worse outcomes. Correction
 of anemia may be useful in improving heart failure outcomes. However, the causes of anemia in heart failure are not entirely
 clear. Specific causes of anemia such as hematinic abnormalities are seen only in a minority of subjects. Renal dysfunction
 and neurohormonal and proinflammatory cytokine activation appear to contribute to anemia of chronic disease in the majority
 of the patients, re...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1195770</comments>
            <pubDate>Thu, 31 Jan 2008 15:50:55 +0100</pubDate>
            <guid isPermaLink="false">1195770</guid>        </item>
        <item>
            <title>Erythropoietin: physiology and molecular mechanisms</title>
            <link>http://www.medworm.com/index.php?rid=1195769&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F7j11x433m7378390%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Erythropoietin, the primary regulator of erythropoiesis, is produced by the kidney and levels vary inversely with oxygen availability.
 Hypoxia-inducible factor-1 (HIF-1), a major transcriptional regulator of several hypoxia-sensitive genes, including erythropoietin,
 is functionally deactivated by oxygen in a reaction catalyzed by prolyl hydroxylase. Erythropoietin acts by binding to a specific
 trans-membrane dimeric receptor which has been found in erythroid and non-erythroid cell types. The interaction between erythropoietin
 and its receptor ultimately leads to conformational change and phosphorylation of the receptor and expression of genes coding
 for proteins that are anti-apoptotic. Development of erythropoietin stimulating agents is an area of active research....</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1195769</comments>
            <pubDate>Thu, 31 Jan 2008 15:50:54 +0100</pubDate>
            <guid isPermaLink="false">1195769</guid>        </item>
        <item>
            <title>Do non-hemopoietic effects of erythropoietin play a beneficial role in heart failure?</title>
            <link>http://www.medworm.com/index.php?rid=1195768&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fxkq2371v51168g42%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Erythropoietin (EPO) is not solely a hormone charged with regulating the proliferation and differentiation of erythroid cells.
 Indeed, EPO is synthesized locally by many cells, especially under conditions of stress or injury. In these paracrine/autocrine
 settings, EPO plays a crucial protective–restorative role, activating cytoprotection (e.g., in the brain, heart, and kidney),
 reducing inflammatory responses, preserving vascular integrity, and mobilizing stem cells, including proliferation and differentiation
 of endothelial progenitor cells. EPO administration prevents cardiac myocyte apoptosis and decreases infarct size in several
 studies using rodent models of myocardial infarction. Recently, some key steps of the signaling pathways by which EPO confers
 cardi...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1195768</comments>
            <pubDate>Thu, 31 Jan 2008 15:50:54 +0100</pubDate>
            <guid isPermaLink="false">1195768</guid>        </item>
        <item>
            <title>The use of cognitive behavioral therapy in the treatment of depression for individuals with CHF</title>
            <link>http://www.medworm.com/index.php?rid=1191086&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fw02k38831757rt6t%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Patients diagnosed with CHF have disproportionately high rates of depression. Research has demonstrated significant consequences
 of depression in patients with CHF including poor quality of life, worse medical adherence and increased health complications,
 health care utilization, and medical costs. Despite these consequences, the treatment of depression in patients with CHF has
 not been widely explored. In fact, a review of the literature demonstrates a clear gap when it comes to efficacious treatments
 of depression in patients afflicted with CHF. The present article introduces the empirically supported therapy ‘cognitive
 behavioral therapy’ (CBT) and provides information about the literature supporting the use of CBT in depressed patients. Finally,
 the presen...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1191086</comments>
            <pubDate>Tue, 29 Jan 2008 15:49:14 +0100</pubDate>
            <guid isPermaLink="false">1191086</guid>        </item>
        <item>
            <title>Apoptosis: a potentially reversible, meta-stable state of the heart</title>
            <link>http://www.medworm.com/index.php?rid=1184304&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fr12134h328003485%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Heart failure (HF) is a major problem worldwide, but its pathogenesis remains unclear. Apoptosis or programmed cell death
 is thought to play a crucial role in its progression. While primarily thought to be a method for cardiomyocyte loss, provocative
 newer data suggest that the apoptotic cell is not inevitably committed to death. Apoptosis might be one of the meta-stable
 transition states, like the hibernating myocardium, that may be reversible with appropriate therapy. The cell with activated
 apoptotic machinery is likely to contribute to reversible systolic dysfunction while awaiting its ultimate fate. We will briefly
 review some of the data to support such a concept. If proven correct, this may change our future preventive and therapeutic
 strategies. Methods to...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1184304</comments>
            <pubDate>Thu, 24 Jan 2008 16:57:07 +0100</pubDate>
            <guid isPermaLink="false">1184304</guid>        </item>
        <item>
            <title>LVAD destination therapy: applying what we know about psychiatric evaluation and management from cardiac failure and transplant</title>
            <link>http://www.medworm.com/index.php?rid=1184303&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F22222862777347j5%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Left ventricular assist devices (LVADs) have evolved into long-term use as destination therapy for those with severe end-stage
 heart failure due to other medical risks. Success with LVAD depends on adherence to a complicated mechanical regimen, and
 acceptance of a life that is far from normal. Patients with LVADs share characteristics with other end-stage cardiac failure
 patients and those waiting for or receiving heart transplants. Understanding the more thoroughly studied issues of psychiatric
 disorders, adherence, and behavioral correlates of success in heart failure and transplantation may identify feasible strategies
 for optimizing care of LVAD patients and suggest directions for future research. Depression and distress complicate post-transplant
 care. Psychi...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1184303</comments>
            <pubDate>Thu, 24 Jan 2008 16:57:07 +0100</pubDate>
            <guid isPermaLink="false">1184303</guid>        </item>
        <item>
            <title>Hypertension, RAS, and gender: what is the role of aminopeptidases?</title>
            <link>http://www.medworm.com/index.php?rid=1184305&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh3104715k084wp45%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Hypertension is the major risk factor for coronary heart disease, stroke, and renal disease. Also, it is probably the most
 important risk factor for peripheral vascular disease and vascular dementia. Although hypertension occurs in both men and
 women, gender differences have been observed. However, whether sex hormones are responsible for the observed gender-associated
 differences in arterial blood pressure, and which is their mechanism of action, remains unclear. Local and circulating renin–angiotensin
 systems (RAS) are examples of systems that may be involved in the pathogenesis of hypertension. Classically, angiotensin II
 (Ang II) has been considered as the effector peptide of the RAS, but Ang II is not the only active peptide. Several of its
 degradation prod...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1184305</comments>
            <pubDate>Thu, 24 Jan 2008 16:57:06 +0100</pubDate>
            <guid isPermaLink="false">1184305</guid>        </item>
        <item>
            <title>Introduction—cell death in heart failure</title>
            <link>http://www.medworm.com/index.php?rid=1184302&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F960838872216m812%2F</link>
            <description>Content Type Journal ArticleDOI 10.1007/s10741-008-9080-3Authors
		Richard N. Kitsis, Albert Einstein College of Medicine Departments of Medicine and Cell Biology, Cardiovascular Research Center, and Cancer Center Forchheimer G46, 1300 Morris Park Avenue Bronx NY 10461 USAJagat Narula, University of California, Irvine School of Medicine Division of Cardiology 101 The City Drive, Bldg. 53, Mail Route 81, Orange Irvine CA 92868 4080 USA
	

	
		Journal Heart Failure ReviewsOnline ISSN 1573-7322Print ISSN 1382-4147 (Source: Heart Failure Reviews)</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1184302</comments>
            <pubDate>Thu, 24 Jan 2008 16:57:06 +0100</pubDate>
            <guid isPermaLink="false">1184302</guid>        </item>
        <item>
            <title>The significance of brain aminopeptidases in the regulation of the actions of angiotensin peptides in the brain</title>
            <link>http://www.medworm.com/index.php?rid=1145567&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fl71r715r18715476%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;From the outset, the concept of a brain renin-angiotensin system (RAS) has been controversial and this controversy continues
 to this day. In addition to the unresolved questions as to the means by which, and location(s) where brain Ang II is synthesized,
 and the uncertainties regarding the functionality of the different subtypes of Ang II receptors in the brain, a new controversy
 has arisen with respect to the identity of the angiotensin peptide(s) that activate brain AT1 receptors. While it has been known for some time that Ang III can activate Ang II receptors with equivalent or near-equivalent
 efficacy to Ang II, it has been proposed that in the brain, only Ang III is active. This proposal, which we have named “The
 Angiotensin III Hypothesis” states that Ang...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1145567</comments>
            <pubDate>Fri, 11 Jan 2008 16:20:36 +0100</pubDate>
            <guid isPermaLink="false">1145567</guid>        </item>
        <item>
            <title>Mitochondrial centrality in heart failure</title>
            <link>http://www.medworm.com/index.php?rid=1145568&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F22v16w6673w80t10%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;A number of observations have shown that mitochondria are at the center of the pathophysiology of the failing heart and mitochondrial-based
 oxidative stress (OS), myocardial apoptosis, and cardiac bioenergetic dysfunction are implicated in the progression of heart
 failure (HF), as shown by both clinical studies and animal models. In this manuscript, we review the body of evidence that
 multiple defects in mitochondria are central and primary to HF progression. In addition, novel approaches to therapeutic targeting
 of mitochondrial bioenergetic, biogenic, and signaling abnormalities that can impact HF are discussed.
 
	Content Type Journal ArticleDOI 10.1007/s10741-007-9079-1Authors
		José Marín-García, The Molecular Cardiology and Neuromuscular Institute 75 Rarita...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1145568</comments>
            <pubDate>Thu, 10 Jan 2008 16:39:44 +0100</pubDate>
            <guid isPermaLink="false">1145568</guid>        </item>
        <item>
            <title>Programmed cell death in cardiac myocytes: strategies to maximize post-ischemic salvage</title>
            <link>http://www.medworm.com/index.php?rid=1139437&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc884q85v20953250%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The most common cause of systolic dysfunction in the United States is prior ischemic injury. As the basic functional unit
 of the myocardium, the cardiac myocyte is the ultimate target of both the pathogenesis and possible therapies in this paradigm.
 Maintaining adequate numbers of these terminally differentiated units in the myocardium has been the focus of all therapies
 in ischemic syndromes, including reperfusion strategies. Programmed cell death, in the forms of apoptosis, necrosis and possibly,
 autophagic cell death are the final arbiters of myocyte numbers following myocardial infarction. This review will focus on
 the evidence for cell death in the development of heart failure following myocardial infarction, a brief review of the relevant
 pathways and the ta...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1139437</comments>
            <pubDate>Sun, 06 Jan 2008 14:56:56 +0100</pubDate>
            <guid isPermaLink="false">1139437</guid>        </item>
        <item>
            <title>Aminopeptidase A inhibitors as centrally acting antihypertensive agents</title>
            <link>http://www.medworm.com/index.php?rid=1139438&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Flp88v0806344800n%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Among the main bioactive peptides of the brain renin–angiotensin system, angiotensin (Ang) II and AngIII exhibit the same
 affinity for the type 1 and type 2 Ang receptors. Both peptides, injected intracerebroventricularly, cause similar increase
 in blood pressure (BP). Because AngII is converted in&amp;nbsp;vivo to AngIII, the identity of the true effector is unknown. This review
 summarized recent insights into the predominant role of brain AngIII in the central control of BP underlining the fact that
 brain aminopeptidase A (APA), the enzyme forming central AngIII, could constitute a putative central therapeutic target for
 the treatment of hypertension. This led to the development of potent, systematically active APA inhibitors, such as RB150,
 as a prototype of a ne...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1139438</comments>
            <pubDate>Fri, 04 Jan 2008 19:51:02 +0100</pubDate>
            <guid isPermaLink="false">1139438</guid>        </item>
        <item>
            <title>Ultrastructural definition of apoptosis in heart failure</title>
            <link>http://www.medworm.com/index.php?rid=1130640&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fw2754621278m1650%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Cardiac myocytes die through apoptosis, oncosis, and autophagy. Apoptosis affects single cells and is morphologically characterized
 by nuclear fragmentation with generation of apoptotic bodies that can be seen either within dying cells or free in the interstitial
 spaces. Dead myocytes are removed by macrophages through phagocytosis without triggering inflammation. The circulating markers
 of myocyte necrosis are not increased by apoptosis. The morphologic changes of the induction and early execution phases are
 seen at electron microscopy while late fragmentation is visible on both light and electron microscopy. Immunoelectron microscopy
 provides combined functional and structural information showing cytochrome c immuno-labelling release from mitochondria, TUNEL labe...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1130640</comments>
            <pubDate>Thu, 03 Jan 2008 16:30:20 +0100</pubDate>
            <guid isPermaLink="false">1130640</guid>        </item>
        <item>
            <title>Introduction: aminopeptidases and hypertension—mechanisms of action and therapeutic strategies</title>
            <link>http://www.medworm.com/index.php?rid=1117369&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F57j1041192072854%2F</link>
            <description>Content Type Journal ArticleDOI 10.1007/s10741-007-9076-4Authors
		John W. Wright, Stadium Way Pullman 99164-4820 USA
	

	
		Journal Heart Failure ReviewsOnline ISSN 1573-7322Print ISSN 1382-4147 (Source: Heart Failure Reviews)</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1117369</comments>
            <pubDate>Tue, 25 Dec 2007 16:00:11 +0100</pubDate>
            <guid isPermaLink="false">1117369</guid>        </item>
        <item>
            <title>Simplified apoptotic cascades</title>
            <link>http://www.medworm.com/index.php?rid=1099890&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F16145410741qtp20%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Apoptosis is an evolutionarily conserved mode of cell death that is tightly regulated and critical for multicellular organism
 development and cellular homeostasis. Specific biochemical and morphological changes characterise cells undergoing apoptosis,
 and reflect the specificity in which activated apoptotic pathways follow. The two best-characterized apoptotic pathways are
 the extrinsic pathway and the intrinsic pathway, which involve cell surface death receptors and the mitochondria and endoplasmic
 reticulum respectively. Apoptotic stimuli lead to activation of either or both of these pathways, and involve sequential activation
 of different cysteine proteases (caspases), and in the case of the intrinsic pathway, activation of a family of Bcl-2 proteins
 that criti...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1099890</comments>
            <pubDate>Sat, 15 Dec 2007 19:38:35 +0100</pubDate>
            <guid isPermaLink="false">1099890</guid>        </item>
        <item>
            <title>Intervention for apoptosis in cardiomyopathy</title>
            <link>http://www.medworm.com/index.php?rid=1097106&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc4lx6815806107m6%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Apoptosis plays an important role in pathogenesis of primary and secondary cardiomyopathies. It is proposed that antiapoptotic
 interventions may constitute an effective strategy for these diseases. Some of the antiapoptotic interventions are “old wine
 in a new bottle” measures already included in the conventional pharmacotherapy. As specific antiapoptotic treatment, caspase
 inhibitors and anti-TNF-α antibody are in early phases of clinical trials in non-cardiac diseases or being contemplated for
 clinical studies. Non-pharmacotherapies such as cardiac resynchronization and left ventricular assist device also exert cardioprotection
 partly by antiapoptotic mechanisms. In the field of regenerative medicine, myocardial transplantation of bone marrow-derived
 stem c...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1097106</comments>
            <pubDate>Fri, 14 Dec 2007 15:55:43 +0100</pubDate>
            <guid isPermaLink="false">1097106</guid>        </item>
        <item>
            <title>Noninvasive imaging of apoptosis in cardiovascular disease</title>
            <link>http://www.medworm.com/index.php?rid=1092814&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fpuql1q51q547629h%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Recent advances in molecular imaging have permitted the noninvasive imaging of apoptosis, a critical process underlying the
 pathogenesis of many diseases of the cardiovascular system including atherosclerotic vascular disease, myocardial ischemia
 and reperfusion injury, chronic heart failure, myocarditis, and cardiac allograft rejection. Multiple molecular targets including
 phosphatidylserine, phosphatidylinositol 3-kinase, and caspases have been targeted by a variety of imaging agents and modalities
 such as nuclear scintigraphy, PET, MRI, and fluorescent and bioluminescent imaging. Translationally, methods utilizing radiolabeled
 annexin V have proven promising in several clinical trials of ischemia-reperfusion injury and cardiac allograft rejection.
 New approache...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1092814</comments>
            <pubDate>Wed, 12 Dec 2007 15:38:58 +0100</pubDate>
            <guid isPermaLink="false">1092814</guid>        </item>
        <item>
            <title>Symptom perception in CHF: (why mind matters)</title>
            <link>http://www.medworm.com/index.php?rid=1090216&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc24033j4542ht3gx%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Symptoms utilized in the clinical care of heart failure as markers of disease severity include, dyspnea, insomnia, low energy,
 fatigue, poor appetite, and diminished memory. This is despite the fact that physiologic variables such as cardiac ejection
 fraction and oxygen consumption do not accurately predict functional state in individuals with congestive heart failure (CHF).
 Distress (anxiety and depression) may amplify symptom complaints without associated physiologic aberration. Personality traits
 and psychiatric illness, such as mood, anxiety, and psychotic illnesses may also alter perception of somatic symptoms that
 are associated with this chronic illness. The impact of distress and its treatment on functional performance and CHF symptom
 reporting deserve add...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1090216</comments>
            <pubDate>Tue, 11 Dec 2007 15:36:23 +0100</pubDate>
            <guid isPermaLink="false">1090216</guid>        </item>
        <item>
            <title>Alcohol use and congestive heart failure: incidence, importance, and approaches to improved history taking</title>
            <link>http://www.medworm.com/index.php?rid=1047523&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fy7m648737h106200%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Alcohol use, abuse, and dependence have the potential to result in alcoholic cardiomyopathy (ACM). This distinct form of congestive
 heart failure (CHF) is responsible for 21–36% of all cases of nonischemic dilated cardiomyopathy in Western society. Without
 complete abstinence, the 4-year mortality for ACM approaches 50%. Therefore, accurate and detailed assessment of alcohol use
 in congestive heart failure is essential. The prevalence of problematic alcohol use is unrecognized by many clinicians. Clinical
 assessment of alcohol intake is often reduced to a simple question such as, “Do you drink?” Denial and minimization are hallmarks
 of alcohol abuse, with many individuals underreporting their use of alcohol. Clinicians can overcome these hurdles by implementi...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1047523</comments>
            <pubDate>Thu, 22 Nov 2007 16:31:55 +0100</pubDate>
            <guid isPermaLink="false">1047523</guid>        </item>
        <item>
            <title>Adherence to exercise training in heart failure: a review</title>
            <link>http://www.medworm.com/index.php?rid=1039678&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fyg4228x384477446%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Exercise training is increasingly recognized as a viable treatment option for patients with heart failure (HF). For exercise
 to be a maximally effective treatment, it is important that patients adhere to the exercise prescription. In this review,
 the current state of adherence monitoring and intervention in randomized HF trials will be summarized, along with recommendations
 for advancing understanding of adherence in this population. Barriers to exercise participation and strategies to enhance
 adherence to exercise-training programs will be explored. Finally, directions for future research on exercise adherence in
 HF patients will be provided.
 
	Content Type Journal ArticleDOI 10.1007/s10741-007-9054-xAuthors
		Krista A. Barbour, Duke University Medical Center Dep...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1039678</comments>
            <pubDate>Fri, 16 Nov 2007 16:02:19 +0100</pubDate>
            <guid isPermaLink="false">1039678</guid>        </item>
        <item>
            <title>Aminopeptidase N in arterial hypertension</title>
            <link>http://www.medworm.com/index.php?rid=1039679&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fp55215746v7v6115%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Aminopeptidase N (APN) or CD13 is a conserved type II integral membrane zinc-dependent metalloprotease in the M1 family of
 ectoenzymes. APN is abundant in the kidneys and central nervous system. Identified substrates include Angiotensin III (Ang
 III); neuropeptides, including enkephalins and endorphins; and homones, including kallidan and somatostatin. It is developmentally
 expressed, a myelomonocytic marker for leukemias, and a receptor for coronovirus. There is evolving support for APN in the
 regulation of arterial blood pressure and the pathogenesis of hypertension. In rodent strains, intracerebraventricular (i.c.v.)
 infusions of APN reduces, while inhibitors of APN activity have a pressor effect on blood pressure. Dysregulation of central
 APN has been linked t...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1039679</comments>
            <pubDate>Fri, 16 Nov 2007 16:02:18 +0100</pubDate>
            <guid isPermaLink="false">1039679</guid>        </item>
        <item>
            <title>Biochemical and enzymatic properties of the M1 family of aminopeptidases involved in the regulation of blood pressure</title>
            <link>http://www.medworm.com/index.php?rid=1026779&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fwlg3453h3q68t405%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;It is becoming evident that several aminopeptidases belonging to the M1 family such as aminopeptidase A (APA), placental leucine
 aminopeptidase (P-LAP), and adipocyte-derived leucine aminopeptidase (A-LAP) play important roles in the regulation of blood
 pressure under both the physiological and pathological conditions. They share HEXXH(X)18E zinc-binding and GAMEN motifs essential for enzymatic activities. In this review, the current situation regarding the biochemical
 characteristics of these enzymes including enzymatic properties and modes of action is summarized.
 
	Content Type Journal ArticleDOI 10.1007/s10741-007-9064-8Authors
		Masafumi Tsujimoto, RIKEN Laboratory of Cellular Biochemistry 2-1 Hirosawa, Wako-shi Saitama 351-0198 JapanYoshikuni Goto, RIKEN Labor...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1026779</comments>
            <pubDate>Tue, 13 Nov 2007 16:16:36 +0100</pubDate>
            <guid isPermaLink="false">1026779</guid>        </item>
        <item>
            <title>Involvement of insulin-regulated aminopeptidase in the effects of the renin–angiotensin fragment angiotensin IV: a review</title>
            <link>http://www.medworm.com/index.php?rid=1017048&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F156u768345jl7007%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;For decades, angiotensin (Ang) II was considered as the end product and the only bioactive peptide of the renin–angiotensin
 system (RAS). However, later studies revealed biological activity for other Ang fragments. Amongst those, Ang IV has drawn
 a lot of attention since it exerts a wide range of central and peripheral effects including the ability to enhance learning
 and memory recall, anticonvulsant and anti-epileptogenic properties, protection against cerebral ischemia, activity at the
 vascular level and an involvement in atherogenesis. Some of these effects are AT1 receptor dependent but others most likely result from the binding of Ang IV to insulin-regulated aminopeptidase (IRAP) although
 the exact mechanism(s) of action that mediate the Ang IV-induced effe...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1017048</comments>
            <pubDate>Thu, 08 Nov 2007 16:09:59 +0100</pubDate>
            <guid isPermaLink="false">1017048</guid>        </item>
        <item>
            <title>New insights into the importance of aminopeptidase A in hypertension</title>
            <link>http://www.medworm.com/index.php?rid=1017047&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F9164w50326mqx141%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The renin-angiotensin system (RAS) plays an important role in the maintenance of normal blood pressure and the etiology of
 hypertension; however, minimal attention has been paid to the degradation of the effector peptide, angiotensin II (AngII).
 Since aminopeptidase A (APA)-deficient mice develop hypertension APA appears to be an essential enzyme in the control of blood
 pressure via degradation of AngII. The robust hypertension seen in the spontaneously hypertensive rat (SHR) is due to activation
 of the RAS, and an accompanying decrease in kidney APA. Changes in APA have also been measured during the activation of the
 RAS in the Goldblatt hypertension model and Dahl salt-sensitive (DSS) rat. The DSS rat shows an elevation in renal APA activity
 at the onset of hype...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1017047</comments>
            <pubDate>Thu, 08 Nov 2007 16:09:59 +0100</pubDate>
            <guid isPermaLink="false">1017047</guid>        </item>
        <item>
            <title>The clinical and research applications of aerobic capacity and ventilatory efficiency in heart failure: an evidence-based review</title>
            <link>http://www.medworm.com/index.php?rid=1017050&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F5q2r14r5612j1m30%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;A hallmark symptom of heart failure (HF) is exercise intolerance, typically evidenced by excessive shortness of breath, and/or
 fatigue with exertion. In recent years, the physiologic response to progressive exercise using direct measures of ventilation
 and gas exchange, commonly termed the cardiopulmonary exercise test (CPX), has evolved into an important clinical tool in
 the management of patients with HF. There is currently debate regarding the optimal CPX response to apply when stratifying
 risk for mortality, hospitalization, or other outcomes in patients with HF. Early studies in this area focused on the application
 of peak VO2 in predicting outcomes in patients considered for transplantation. More recently, the focus of these studies has shifted
 to an emphasi...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1017050</comments>
            <pubDate>Wed, 07 Nov 2007 15:22:57 +0100</pubDate>
            <guid isPermaLink="false">1017050</guid>        </item>
        <item>
            <title>Pathways involved in the transition from hypertension to hypertrophy to heart failure. Treatment strategies</title>
            <link>http://www.medworm.com/index.php?rid=1017049&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fv0t7j72601024v28%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The renin-angiotensin-aldosterone system (RAAS) is critical in regulating systemic blood pressure, water and electrolyte balance,
 and pituitary gland hormones. These physiologies appear to be primarily mediated by the angiotensin II/AT1 receptor subtype system. Overstimulation of this system can predispose cardiovascular disease (CVD) characterized by excessive
 vasoconstriction, fibrosis, and cardiac remodeling. If untreated, the patient typically displays a continuum of pathophysiologic
 conditions progressing from atherosclerosis to left ventricle hypertrophy (LVH), coronary thrombosis, myocardial infarcts,
 with heart failure as an endpoint. Intervention with antihypertensive therapy is necessary to inhibit this progression. RAAS
 blocking drugs appear to be the mo...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1017049</comments>
            <pubDate>Wed, 07 Nov 2007 15:22:57 +0100</pubDate>
            <guid isPermaLink="false">1017049</guid>        </item>
        <item>
            <title>Exercise training in patients with heart failure: clinical outcomes, safety, and indications</title>
            <link>http://www.medworm.com/index.php?rid=981885&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fy1273605301602h6%2F</link>
            <description>This article reviews the effects of exercise training on clinical outcomes and addressing the safety of exercise
 training and the indications for training in HF patients.
 
	Content Type Journal ArticleDOI 10.1007/s10741-007-9052-zAuthors
		Robert S. McKelvie, Hamilton Health Sciences Corporation – General Site 237 Barton Street East L8L 2X2 Hamilton ON Canada
	

	
		Journal Heart Failure ReviewsOnline ISSN 1573-7322Print ISSN 1382-4147 (Source: Heart Failure Reviews)</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=981885</comments>
            <pubDate>Thu, 25 Oct 2007 15:07:03 +0100</pubDate>
            <guid isPermaLink="false">981885</guid>        </item>
        <item>
            <title>Implications of chronic heart failure on peripheral vasculature and skeletal muscle before and after exercise training</title>
            <link>http://www.medworm.com/index.php?rid=978854&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F33461k825888175u%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;&amp;nbsp;The pathophysiology of chronic heart failure (CHF) is typically conceptualized in terms of cardiac dysfunction. However,
 alterations in peripheral blood flow and intrinsic skeletal muscle properties are also now recognized as mechanisms for exercise
 intolerance that can be modified by therapeutic exercise. This overview focuses on blood delivery, oxygen extraction and
 utilization that result from heart failure. Related features of inflammation, changes in skeletal muscle signaling pathways,
 and vulnerability to skeletal muscle atrophy are discussed. Specific focus is given to the ways in which perfusion and skeletal
 muscle properties affect exercise intolerance and how peripheral improvements following exercise training increase aerobic
 capacity. We also ide...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=978854</comments>
            <pubDate>Tue, 23 Oct 2007 14:39:33 +0100</pubDate>
            <guid isPermaLink="false">978854</guid>        </item>
        <item>
            <title>Treatment of depression in patients with congestive heart failure</title>
            <link>http://www.medworm.com/index.php?rid=978853&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fb2140437w433j334%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Heart failure is common, and depression is common in heart failure patients, adding substantially to the burden of the disease.
 There is some evidence for the safe and at least modestly effective use of psychotherapy and antidepressants to treat depression
 in heart failure patients. Cognitive behavioral psychotherapy and selective serotonin reuptake inhibitors are first line treatments.
 The efficacy of depression treatment in altering cardiac outcomes in heart failure patients has yet to be established.
 
	Content Type Journal ArticleDOI 10.1007/s10741-007-9058-6Authors
		Peter A. Shapiro, New York Presbyterian Hospital-Columbia University Medical Center, Columbia University Department of Psychiatry 622 W. 168 St. Box 427 New York NY 10032 USA
	

	
		Journal Heart Fa...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=978853</comments>
            <pubDate>Tue, 23 Oct 2007 14:39:32 +0100</pubDate>
            <guid isPermaLink="false">978853</guid>        </item>
        <item>
            <title>Principles of exercise prescription for patients with chronic heart failure</title>
            <link>http://www.medworm.com/index.php?rid=958655&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F01v633g54022nk25%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Chronic heart failure (CHF) is a common and debilitating condition characterized by reduced exercise tolerance. While exercise
 training was once thought to be contraindicated for patients with CHF, a substantial body of data has been published over
 the last two decades to support the use of exercise programs for these patients. Improvements in exercise capacity, quality
 of life, and mortality have been demonstrated among patients with CHF who have participated in formal exercise programs. Exercise prescription is a means of assessing and interpreting clinical information and applying the principles of training to develop an appropriate
 regimen so that these benefits are achieved. The major principles of the exercise prescription are the mode, frequency, duration, an...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=958655</comments>
            <pubDate>Tue, 16 Oct 2007 15:38:31 +0100</pubDate>
            <guid isPermaLink="false">958655</guid>        </item>
        <item>
            <title>Central adaptations to exercise training in patients with chronic heart failure</title>
            <link>http://www.medworm.com/index.php?rid=951849&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fp2714h086424q593%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;In chronic heart failure patients, the increase of peak VO2 observed after a period of aerobic training is currently attributed more to peripheral (skeletal muscle) than central (heart)
 adaptations. This paper reviews the current scientific evidence regarding the existence or the absence of significant training-induced
 adaptations of peak cardiac output and its determinants in patients with chronic heart failure due to left ventricular systolic
 dysfunction. It is concluded that, on the basis of available literature, a training-induced significant increase of peak cardiac
 output with respect to pre-training values does exist in the chronic heart failure population. Such an effect is due to adaptations
 of the main cardiac output determinants, that is, heart rate and ...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=951849</comments>
            <pubDate>Fri, 12 Oct 2007 17:54:59 +0100</pubDate>
            <guid isPermaLink="false">951849</guid>        </item>
        <item>
            <title>Resistance exercise: training adaptations and developing a safe exercise prescription</title>
            <link>http://www.medworm.com/index.php?rid=951848&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F71101813x7245334%2F</link>
            <description>This article presents evidence that improvement of skeletal muscle phenotype (muscle mass, fiber morphology,
 and histochemistry) should be a fundamental goal of rehabilitation in patients with CHF. Moreover, RT may be the preferred
 exercise modality when targeting the periphery for muscle phenotype adaptation.
 
	Content Type Journal ArticleDOI 10.1007/s10741-007-9055-9Authors
		Randy W. Braith, University of Florida Center for Exercise Science, College of Health and Human Performance and the College of Medicine P.O. Box 118206 Gainesville FL 32611 USADarren T. Beck, University of Florida Center for Exercise Science, College of Health and Human Performance and the College of Medicine P.O. Box 118206 Gainesville FL 32611 USA
	

	
		Journal Heart Failure ReviewsOnline ISSN 1573-7322Print I...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=951848</comments>
            <pubDate>Fri, 12 Oct 2007 17:54:59 +0100</pubDate>
            <guid isPermaLink="false">951848</guid>        </item>
        <item>
            <title>Adaptations in autonomic function during exercise training in heart failure</title>
            <link>http://www.medworm.com/index.php?rid=951847&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ff475826k41903u23%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Although neurohumoral excitation is the hallmark of heart failure (HF), the mechanisms underlying this alteration are not
 entirely known. Abnormalities in several systems contribute to neurohumoral excitation in HF, including arterial and cardiopulmonary
 baroreceptors, central and peripheral chemoreceptors, cardiac chemoreceptors, and central nervous system abnormalities. Exercise
 intolerance is characteristic of chronic HF, and growing evidence strongly suggests that exercise limitation in patients with
 chronic HF is not due to elevated filling pressures or inadequate cardiac output during exercise, but instead due to skeletal
 myopathy. Several lines of evidence suggest that sympathetic excitation contributes to the skeletal myopathy of HF, since
 sympathetic acti...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=951847</comments>
            <pubDate>Fri, 12 Oct 2007 17:54:59 +0100</pubDate>
            <guid isPermaLink="false">951847</guid>        </item>
        <item>
            <title>Effects of exercise training on inflammatory markers in patients with heart failure</title>
            <link>http://www.medworm.com/index.php?rid=938494&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fa873111q54743215%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Cardiologists now recognize that the cardio-centric model of heart failure does not sufficiently explain the entire traits
 particular to chronic heart failure. Evidence accumulates, that many features of the syndrome can be explained by the known
 biological effects of inflammatory mediators. Indeed, when expressed in experimental models at concentrations commonly observed
 in heart failure, inflammatory mediators such as tumor necrosis factor-α, interleukin-6, and nitric oxide can produce effects
 that mimic features of heart failure, including (but not limited to) progressive left-ventricular dysfunction, pulmonary edema,
 left-ventricular remodeling, and cardiomyopathy. As we witness anti-cytokine therapies and other strategies to avoid an increase
 in cytokines we...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=938494</comments>
            <pubDate>Sat, 06 Oct 2007 17:41:31 +0100</pubDate>
            <guid isPermaLink="false">938494</guid>        </item>
        <item>
            <title>Introduction: exercise in patients with chronic heart failure</title>
            <link>http://www.medworm.com/index.php?rid=932484&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fr543g3587628n427%2F</link>
            <description>Content Type Journal ArticleDOI 10.1007/s10741-007-9049-7Authors
		Steven J. Keteyian, Henry Ford Hospital Division of Cardiovascular Medicine 6525 Second Avenue Detroit MI 48202 USAWilliam E. Kraus, Duke University Medical Center Division of Cardiovascular Medicine Durham NC USA
	

	
		Journal Heart Failure ReviewsOnline ISSN 1573-7322Print ISSN 1382-4147 (Source: Heart Failure Reviews)</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=932484</comments>
            <pubDate>Fri, 05 Oct 2007 15:57:58 +0100</pubDate>
            <guid isPermaLink="false">932484</guid>        </item>
        <item>
            <title>Should a statin be prescribed to every patient with heart failure?</title>
            <link>http://www.medworm.com/index.php?rid=799917&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fp52014r5k7855046%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Chronic heart failure (HF) represents an emerging epidemic since its prevalence is continuously increasing despite advances
 in treatment. Many recent clinical studies have clearly demonstrated that statin therapy is associated with improved outcomes
 in HF irrespective of aetiology (ischaemic or not) or baseline cholesterol levels. Indeed, most of the conducted large statin
 trials and trials in HF have demonstrated a positive effect of statins in HF patients. Furthermore, the use of statins in
 HF seems to be safe as none of the recent trials has resulted in worse outcomes for HF patients treated with statins. Potential
 mechanisms through which statins could benefit the failing myocardium include non-sterol effects of statins, as well as effects
 on nitric oxide and ...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=799917</comments>
            <pubDate>Mon, 13 Aug 2007 21:49:50 +0100</pubDate>
            <guid isPermaLink="false">799917</guid>        </item>
        <item>
            <title>Drugs, gene transfer, signaling factors: a bench to bedside approach to myocardial stem cell therapy</title>
            <link>http://www.medworm.com/index.php?rid=774003&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc366l14kj585t2rg%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;In the past few years, the dogma that the heart is a terminally differentiated organ has been challenged. Evidence from preclinical
 investigations emerged that there are cells, even in the heart itself, that may be able to restore impaired cardiac function
 after myocardial infarction. Although the exact mechanisms by which the infarcted heart can be repaired by stem cells are
 not yet fully defined, there is a new optimism among cardiologists that this treatment will prove successful in addressing
 the cause of heart failure after myocardial infarction—myocyte loss. Despite the promising preliminary data of human myocardial
 stem cell trials, scientists have also focused on the possibility of enhancing the underlying mechanisms of stem cell repair
 to gain healthier...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=774003</comments>
            <pubDate>Wed, 01 Aug 2007 06:54:14 +0100</pubDate>
            <guid isPermaLink="false">774003</guid>        </item>
        <item>
            <title>Screening, diagnosis &amp; monitoring of depression/distress in CHF patients</title>
            <link>http://www.medworm.com/index.php?rid=774002&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F435w6tm73m741h5m%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Objective and validated measures of depression/distress (anxiety and anger) are available and readily usable at the bedside
 or in clinic. Foremost among these is the Patient’s Health Questionnaire—an adaptation of DSM IV criteria for Major Depressive
 Disorder that permits administration and scoring by nursing or physician personnel, and quantification of the intensity of
 depression. A score of 10 or greater indicates a need for evaluation/treatment. Because of patient denial/minimization/alexithymia,
 PHQ negatives should undergo further screening by having a spouse or friend complete a depression/distress rating scale. The
 only standardized, normed, and validated spouse/friend scale presently available is the Ketterer Stress Symptom Frequency
 Checklist, which ...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=774002</comments>
            <pubDate>Wed, 01 Aug 2007 06:54:13 +0100</pubDate>
            <guid isPermaLink="false">774002</guid>        </item>
        <item>
            <title>Foreword</title>
            <link>http://www.medworm.com/index.php?rid=724595&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fy454432099814450%2F</link>
            <description>Content TypeJournal Article

	
		JournalHeart Failure ReviewsOnline ISSN 1573-7322Print ISSN 1382-4147 (Source: Heart Failure Reviews)</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=724595</comments>
            <pubDate>Sat, 07 Jul 2007 11:13:09 +0100</pubDate>
            <guid isPermaLink="false">724595</guid>        </item>
        <item>
            <title>HDL and its sphingosine-1-phosphate content in cardioprotection</title>
            <link>http://www.medworm.com/index.php?rid=671237&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fw751h6275613v0r1%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Increasing evidence suggests that High-density lipoproteins (HDL) are a direct cardioprotective agent in the setting of acute
 myocardial ischemia/reperfusion injury, and that this cardioprotection occurs independently of their atheroprotective effect.
 Studies on the involved mechanisms have revealed that the biologically active HDL-compound sphingosine-1-phosphate (S1P) is
 responsible for the beneficial effect of HDL on the myocardium. There appears to be an intricate interplay between known preconditioning
 agents and components of the S1P synthesis machinery in the heart, which makes S1P signalling an attractive downstream convergence
 point of preconditioning and cardioprotection at the level of its G protein-coupled receptors. While local S1P production
 has been...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=671237</comments>
            <pubDate>Thu, 07 Jun 2007 07:49:47 +0100</pubDate>
            <guid isPermaLink="false">671237</guid>        </item>
        <item>
            <title>Myocardial protection in man—from research concept to clinical practice</title>
            <link>http://www.medworm.com/index.php?rid=654154&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh81p18808t477836%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Myocardial protection aims at preventing myocardial tissue loss: (a) In the acute stage, i.e., during primary angioplasty
 in acute myocardial infarction. In this setup, the attenuation of reperfusion injury is the main target. As a “mechanical”
 means, post-conditioning has already been tried in man with encouraging results. Pharmacologic interventions that could be
 of promise are statins, insulin, peptide hormones, including erythropoietin, fibroblast growth factor, and many others. (b)
 The patient with chronic coronary artery disease offers another paradigm, with the target of avoidance of further myocyte
 loss through apoptosis and inflammation. Various pharmacologic agents may prove useful in this context, together with exercise
 and “mechanical” improvem...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=654154</comments>
            <pubDate>Fri, 01 Jun 2007 13:50:45 +0100</pubDate>
            <guid isPermaLink="false">654154</guid>        </item>
        <item>
            <title>The late phase of preconditioning and its natural clinical application—gene therapy</title>
            <link>http://www.medworm.com/index.php?rid=654156&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F91671m10567518l3%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;There is little doubt that the discovery of ischemic preconditioning (PC) has been one of the fundamental milestones in the
 field of ischemic biology in the past 20&amp;nbsp;years. The purpose of this article is to review the pathophysiology and molecular
 basis of the late phase of myocardial PC. The exploitation of late PC for the development of novel gene therapy strategies
 aimed at inducing a permanently preconditioned cardiac phenotype (prophylactic cardioprotection) will also be discussed. Deciphering
 the mechanism of late PC has not only conceptual interest but also a considerable therapeutic implications, since transfer
 of the genes that underlie late PC would be expected to replicate the salubrious effects of this response of the heart to
 stress.
 
	Content Ty...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=654156</comments>
            <pubDate>Fri, 01 Jun 2007 13:50:43 +0100</pubDate>
            <guid isPermaLink="false">654156</guid>        </item>
        <item>
            <title>Reperfusion injury salvage kinase signalling: taking a RISK for cardioprotection</title>
            <link>http://www.medworm.com/index.php?rid=654157&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F128156jj94u28h93%2F</link>
            <description>This article reviews the origins and evolution of the RISK pathway, as part of a potential common cardioprotective
 pathway, which can be activated by an ever-expanding list of agents administered at the time of myocardial reperfusion, as
 well as by IPC and IPost. Preliminary clinical studies have demonstrated myocardial protection with several of these pharmacological
 activators of the RISK pathway in AMI patients undergoing PCI. Through the use of appropriately designed clinical trials,
 guided by the wealth of existing preclinical data, the administration of pharmacological agents which are known to activate
 the RISK pathway, when applied as adjuvant therapy to current myocardial reperfusion strategies for patients presenting with
 an AMI, should lead to improved clinical outcomes in...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=654157</comments>
            <pubDate>Fri, 01 Jun 2007 13:50:41 +0100</pubDate>
            <guid isPermaLink="false">654157</guid>        </item>
        <item>
            <title>Cardioprotection in stunned and hibernating myocardium</title>
            <link>http://www.medworm.com/index.php?rid=654155&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fq610500kk01710m5%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Although myocardial ischemia was once thought to result in irreversible cellular damage, it is now demonstrated that in cardiac
 tissue, submitted to the stress of oxygen and substrate deprivation, endogenous mechanisms of cell survival may be activated.
 These molecular mechanisms result in physiological conditions of adaptation to ischemia, known as myocardial stunning and
 hibernation. These conditions result from a switch in gene and protein expression, which sustains cardiac cell survival in
 a context of oxygen deprivation and during the stress of reperfusion. The pattern of cell survival elicited by ischemia in
 myocardial stunning or hibernation results in the activation of cytoprotective mechanisms that will protect the heart against
 further ischemic damage, a...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=654155</comments>
            <pubDate>Fri, 01 Jun 2007 13:50:40 +0100</pubDate>
            <guid isPermaLink="false">654155</guid>        </item>
        <item>
            <title>Newer mechanical devices in the management of acute heart failure</title>
            <link>http://www.medworm.com/index.php?rid=654158&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fg26p011133552km7%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Heart Failure is the only cardiovascular disease diagnosis increasing in prevalence in the United States. Currently there
 are more than 5&amp;nbsp;million people diagnosed with heart failure in the United States and that population is increasing exponentially.
 Clinical trials in advanced pharmacological therapies have shown a significant value in reducing the morbidity and mortality
 of the disease process. Nevertheless, many patients who are optimally treated with drug therapy continue to progress from
 asymptomatic left ventricular dysfunction to symptomatic and then end-stage heart failure. Beyond drug therapy, devices have
 begun to make a significant impact on symptoms and clinical outcomes in patients, particularly those with more advanced forms
 of heart failure. N...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=654158</comments>
            <pubDate>Fri, 01 Jun 2007 13:50:37 +0100</pubDate>
            <guid isPermaLink="false">654158</guid>        </item>
        <item>
            <title>Reperfusion injury as a therapeutic challenge in patients with acute myocardial infarction</title>
            <link>http://www.medworm.com/index.php?rid=643989&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fb356678q6n2g1825%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Cardiomyocyte death secondary to transient ischemia occurs mainly during the first minutes of reperfusion, in the form of
 contraction band necrosis involving sarcolemmal rupture. Cardiomyocyte hypercontracture caused by re-energisation and pH recovery
 in the presence of impaired cytosolic Ca2+ control as well as calpain-mediated cytoskeletal fragility play prominent roles in this type of cell death. Hypercontracture
 can propagate to adjacent cells through gap junctions. More recently, opening of the mitochondrial permeability transition
 pore has been shown to participate in reperfusion-induced necrosis, although its precise relation with hypercontracture has
 not been established. Experimental studies have convincingly demonstrated that infarct size can be markedly ...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=643989</comments>
            <pubDate>Sat, 26 May 2007 15:05:14 +0100</pubDate>
            <guid isPermaLink="false">643989</guid>        </item>
        <item>
            <title>Postconditioning in man</title>
            <link>http://www.medworm.com/index.php?rid=636256&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fl4260w4r54427147%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Acute myocardial infarction is the leading cause of morbidity and mortality in industrialized countries. Ischemic postconditioning,
 that consists of repeated brief episodes of ischemia-reperfusion performed just after reflow following a prolonged ischemic
 insult, dramatically reduces infarct size in animal models. Recent data indicate that it might involve the activation of the
 PI3-kinase—Akt—eNOS as well as PKC signalling pathways and inhibition of the opening of the permeability transition pore.
 A recent clinical study demonstrated that postconditioning protects the human heart. Repeated brief episodes of inflation-deflation
 of the angioplasty balloon performed immediately after re-opening of the culprit coronary artery reduced infarct size by 36%.
 Additiona...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=636256</comments>
            <pubDate>Thu, 24 May 2007 08:10:47 +0100</pubDate>
            <guid isPermaLink="false">636256</guid>        </item>
        <item>
            <title>Postconditioning: a mechanical maneuver that triggers biological and molecular cardioprotective responses to reperfusion</title>
            <link>http://www.medworm.com/index.php?rid=636257&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F03620112p1j74r54%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Infarct size is determined not only by the duration and severity of ischemia, but also by pathological processes initiated
 at reperfusion (reperfusion injury). Numerous pharmacological strategies have been reported which administer drugs at or just
 before the onset of reperfusion, with subsequent salubrious effects, notably a reduction in infarct size. However, few if
 any of these strategies have become standard of care in the catheterization laboratory setting. Postconditioning, defined
 as repeated brief cycles of reperfusion interrupted by ischemia (or hypoxia) applied at the onset of reperfusion, was recently
 introduced as a mechanical strategy to attenuate reperfusion injury. Postconditioning intervenes only during the first few
 minutes of reperfusion. However...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=636257</comments>
            <pubDate>Wed, 23 May 2007 07:42:44 +0100</pubDate>
            <guid isPermaLink="false">636257</guid>        </item>
        <item>
            <title>Mitochondria and cardioprotection</title>
            <link>http://www.medworm.com/index.php?rid=636261&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fk14n74k6ut060158%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Major factors linking mitochondrial dysfunction with myocardial injury are analyzed along with protective mechanisms elicited
 by endogenous processes and pharmacological treatments. In particular, a reduced rate of ATP hydrolysis and a slight increase
 in ROS formation appear to represent the prevailing components of self-defense mechanisms, especially in the case of ischemic
 preconditioning. These protective processes are activated by signaling pathways, which converge on mitochondria activating
 the mitochondrial KATP channels and/or inhibiting the mitochondrial permeability transition pore. These pathways can also be stimulated by pharmacological
 treatments. Another major goal for cardioprotection is decreasing the burst in mitochondrial ROS formation that charact...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=636261</comments>
            <pubDate>Tue, 22 May 2007 10:10:16 +0100</pubDate>
            <guid isPermaLink="false">636261</guid>        </item>
        <item>
            <title>Fibroblast growth factor-2 and cardioprotection</title>
            <link>http://www.medworm.com/index.php?rid=636263&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fb3225602qk658h60%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Boosting myocardial resistance to acute as well as chronic ischemic damage would ameliorate the detrimental effects of numerous
 cardiac pathologies and reduce the probability of transition to heart failure. Experimental cardiology has pointed to ischemic
 and pharmacological pre- as well as post-conditioning as potent acute cardioprotective manipulations. Additional exciting
 experimental strategies include the induction of true regenerative and/or angiogenic responses to the damaged heart, resulting
 in sustained structural and functional beneficial effects. Fibroblast growth factor-2 (FGF-2), an endogenous multifunctional
 protein with strong affinity for the extracellular matrix and basal lamina and well-documented paracrine, autocrine and intacellular
 modes of act...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=636263</comments>
            <pubDate>Tue, 22 May 2007 10:10:14 +0100</pubDate>
            <guid isPermaLink="false">636263</guid>        </item>
        <item>
            <title>Connexin 43 in ischemic pre- and postconditioning</title>
            <link>http://www.medworm.com/index.php?rid=636260&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F370667560j77778l%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Connexin 43 (Cx43) is the predominant protein forming gap junctions and non-junctional hemichannels in ventricular myocardium,
 but Cx43 is also localized at the inner membrane of cardiomyocyte mitochondria. In cardiomyocytes, Cx43 is involved in the
 formation of reactive oxygen species, which are central to the signal transduction cascade of ischemic preconditioning’s protection.
 Accordingly, genetically-induced or age-related loss of Cx43 abolishes infarct size reduction by ischemic preconditioning.
 Similarly, mitochondrial import inhibition of Cx43 completely blocks infarct size reduction by pharmacological preconditioning
 with diazoxide. In contrast to its importance for preconditioning-induced cardioprotection, Cx43 is not important for infarct
 size reductio...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=636260</comments>
            <pubDate>Tue, 22 May 2007 10:10:12 +0100</pubDate>
            <guid isPermaLink="false">636260</guid>        </item>
        <item>
            <title>Protection of the abnormal heart</title>
            <link>http://www.medworm.com/index.php?rid=636264&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ft68736u451038377%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Myocardial ischemia and reperfusion injury have been extensively investigated in the laboratory mainly in healthy tissues.
 However, in clinical settings, ischemic heart disease coexists with certain illnesses, which could potentially influence the
 response of the myocardium to ischemia and reperfusion. Recent research has revealed that the abnormal heart may not be always
 vulnerable to ischemic injury. Furthermore, the effect of powerful means of protection, such as ischemic preconditioning,
 may not be in operation under certain pathological conditions. With this evidence in mind, the present review will focus on
 the response of the abnormal heart to ischemia and reperfusion, the possible underlying mechanisms, and potential cardioprotective
 strategies.
 
	Content...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=636264</comments>
            <pubDate>Tue, 22 May 2007 10:10:10 +0100</pubDate>
            <guid isPermaLink="false">636264</guid>        </item>
        <item>
            <title>Return to the fetal gene program protects the stressed heart: a strong hypothesis</title>
            <link>http://www.medworm.com/index.php?rid=636258&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fjn12v704720711v4%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;A common feature of the hemodynamically or metabolically stressed heart is the return to a pattern of fetal metabolism. A
 hallmark of fetal metabolism is the predominance of carbohydrates as substrates for energy provision in a relatively hypoxic
 environment. When the normal heart is exposed to an oxygen rich environment after birth, energy substrate metabolism is rapidly
 switched to oxidation of fatty acids. This switch goes along with the expression of “adult” isoforms of metabolic enzymes
 and other proteins. However, the heart retains the ability to return to the “fetal” gene program. Specifically, the fetal
 gene program is predominant in a variety of pathophysiologic conditions including hypoxia, ischemia, hypertrophy, and atrophy.
 A common feature of ...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=636258</comments>
            <pubDate>Tue, 22 May 2007 10:10:07 +0100</pubDate>
            <guid isPermaLink="false">636258</guid>        </item>
        <item>
            <title>Signaling pathways in ischemic preconditioning</title>
            <link>http://www.medworm.com/index.php?rid=636259&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fa6n1r2t008n273j6%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Ischemic preconditioning renders the heart resistant to infarction from ischemia/reperfusion. Over the past two decades a
 great deal has been learned about preconditioning’s mechanism. Adenosine, bradykinin, and opioids act in parallel to trigger
 the preconditioned state and do so by activating PKC. While adenosine couples directly to PKC through the phospholipases,
 bradykinin and opioids do so through a complex pathway that includes in order: phosphatidylinositol 3-kinase (PI3-kinase),
 Akt, nitric oxide synthase, guanylyl cyclase, PKG, opening of mitochondrial KATP channels, and activation of PKC by redox signaling. There are even differences between the opioid and bradykinin coupling
 as the former activates PI3-kinase through transactivation of the epidermal gr...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=636259</comments>
            <pubDate>Tue, 22 May 2007 10:10:04 +0100</pubDate>
            <guid isPermaLink="false">636259</guid>        </item>
        <item>
            <title>Cardioprotective actions of peptide hormones in myocardial ischemia</title>
            <link>http://www.medworm.com/index.php?rid=636262&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F2420p46q57162724%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The myocardium represents a major source of several families of peptide hormones under normal physiological conditions and
 the plasma concentrations of many of these “cardiac peptides” (or related pro-peptide fragments) are substantially augmented
 in many cardiac disease states. In addition to well-characterised endocrine functions of several of the cardiac peptides,
 pleiotropic functions within the myocardium and the coronary vasculature represent a significant aspect of their actions in
 health and disease. Here, we focus specifically on the cardioprotective roles of four major peptide families in myocardial
 ischemia and reperfusion: adrenomedullin, kinins, natriuretic peptides and the urocortins. The patterns of early release of
 all these peptides are consis...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=636262</comments>
            <pubDate>Tue, 22 May 2007 10:10:02 +0100</pubDate>
            <guid isPermaLink="false">636262</guid>        </item>
        <item>
            <title>An introduction to acute heart failure syndromes: definition and classification</title>
            <link>http://www.medworm.com/index.php?rid=622148&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fp63l107w248375v1%2F</link>
            <description>Content TypeJournal Article

	
		JournalHeart Failure ReviewsOnline ISSN 1573-7322Print ISSN 1382-4147 (Source: Heart Failure Reviews)</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=622148</comments>
            <pubDate>Thu, 17 May 2007 07:30:19 +0100</pubDate>
            <guid isPermaLink="false">622148</guid>        </item>
        <item>
            <title>Cardioprotection in females: a role for nitric oxide and altered gene expression</title>
            <link>http://www.medworm.com/index.php?rid=622146&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ff7tj4q316334717h%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;A number of epidemiological and animal studies have suggested a cardioprotective role for estrogen. This review will focus
 on the cardioprotective role of estrogen in ischemia-reperfusion injury. Estrogen binding to receptors can lead to altered
 gene expression and estrogen has been shown to induce expression of a number of genes that have been suggested to be important
 in cardioprotection. Estrogen is reported to increase expression of the plasma membrane glucose transporter GLUT4 and to increase
 carbohydrate metabolism. Estrogen has also been reported to increase mitochondrial biogenesis and to alter mitochondrial generation
 of reactive oxygen species. Estrogen results in upregulation of cardiac eNOS and nNOS, which have been shown previously to
 be important med...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=622146</comments>
            <pubDate>Thu, 17 May 2007 07:30:17 +0100</pubDate>
            <guid isPermaLink="false">622146</guid>        </item>
        <item>
            <title>Preconditioning in humans</title>
            <link>http://www.medworm.com/index.php?rid=622147&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F78k181q08l05483p%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Brief ischemia to the myocardium initiates a cascade of biochemical events in cardiac myocytes that protects the heart muscle
 during subsequent ischemic insults. This phenomenon is called ischemic preconditioning. If an acute myocardial infarction
 is preceded by preinfarction angina, it results in smaller infarction size, fewer cardiac arrhythmias, and better-left ventricular
 function. During coronary intervention, brief balloon inflation protects the heart during subsequent inflations. Patients
 vary in the degree of preconditioning and those patients who have the ability to demonstrate a significant preconditioning
 effect will have lesser incidence of subsequent cardiac events. Preconditioning protects the myocardium during coronary artery
 bypass surgery, particu...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=622147</comments>
            <pubDate>Thu, 17 May 2007 07:30:15 +0100</pubDate>
            <guid isPermaLink="false">622147</guid>        </item>
        <item>
            <title>Non-invasive ventilation</title>
            <link>http://www.medworm.com/index.php?rid=609275&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ffuw3175qt2603n56%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Non-invasive ventilation (NIV) refers to the delivery of mechanical ventilation to the lungs using techniques that do not
 require an endotracheal airway. Essentially, there are two modalities: continuous positive airway pressure (CPAP) and pressure
 support ventilation (NIPSV). In acute pulmonary edema (APE) both modalities have shown a faster improvement in gas exchange
 and physiologic parameters with respect to conventional oxygen therapy.
 
 CPAP is a simple technique that may reduce preload and afterload, increasing cardiac output in some patients. It has been
 successfully used in APE in the last 30&amp;nbsp;years, demonstrating a reduction in the intubation rate and mortality. The most common
 level of pressure is 10&amp;nbsp;cmH2O.
 
 
 
 NIPSV is a more complex mode t...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=609275</comments>
            <pubDate>Thu, 10 May 2007 07:12:48 +0100</pubDate>
            <guid isPermaLink="false">609275</guid>        </item>
        <item>
            <title>Acute heart failure syndromes: clinical scenarios and pathophysiologic targets for therapy</title>
            <link>http://www.medworm.com/index.php?rid=609277&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc8w50404555v7377%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Acute heart failure syndromes (AHFS) represent the most common discharge diagnosis in patients over age 65&amp;nbsp;years, with an
 exceptionally high mortality and readmission rates at 60–90&amp;nbsp;days. Recent surveys and registries have generated important information
 concerning the clinical characteristics of patients with AHFS and their prognosis. Most patients with AHFS present either
 with normal systolic blood pressure or elevated blood pressure. Patients who present with elevated systolic blood pressure
 usually have pulmonary congestion, a relatively preserved left ventricular ejection fraction (LVEF), are often elderly women,
 and their symptoms develop typically and abruptly. Patients with normal systolic blood pressure present with systemic congestion,
 reduce...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=609277</comments>
            <pubDate>Wed, 09 May 2007 14:29:58 +0100</pubDate>
            <guid isPermaLink="false">609277</guid>        </item>
        <item>
            <title>Classical inotropes and new cardiac enhancers</title>
            <link>http://www.medworm.com/index.php?rid=609276&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F472321264g8686m5%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Acute heat failure syndromes are a heterogenous group of conditions. Chronic heart failure exacerbations represent the vast
 majority of cases. Pathophysiologic mechanisms, such as hypotension with peripheral tissue hypoperfusion, renal function impairment
 and myocardial ischemia and injury, adversely affect patients’ clinical outcome. Classical inotropes, such as beta-agonists
 (dobutamine, dopamine) and phosphodiesterase inhibitors (milrinone), seem to improve clinical symptoms and hemodynamics of
 acutely decompensated chronic heat failure patients, but they have been associated with increased long-term mortality. Thus,
 on the basis of the available evidence, these agents can be used only as a temporary treatment of acute heart failure exacerbations
 with stringe...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=609276</comments>
            <pubDate>Wed, 09 May 2007 14:29:55 +0100</pubDate>
            <guid isPermaLink="false">609276</guid>        </item>
        <item>
            <title>Medication adherence in heart failure</title>
            <link>http://www.medworm.com/index.php?rid=609278&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj27387875vv28u40%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Non-adherence with medical regimens in heart failure is a significant challenge and serves as a major reason that favorable
 outcomes associated with various therapies evaluated in clinical trials have not translated to the so-called real-world setting.
 Non-adherence has complex influences and is clearly associated with poorer outcomes. The approaches that are used or have
 been proposed to improve drug-taking behavior, such as in-hospital initiation of therapy, simplification of dosing regimens
 through adoption of combination and long-acting formulations, and improvements in provider–patient communication, are reviewed.
 
	Content TypeJournal Article

	
		JournalHeart Failure ReviewsOnline ISSN 1573-7322Print ISSN 1382-4147 (Source: Heart Failure Reviews)</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=609278</comments>
            <pubDate>Fri, 04 May 2007 09:02:25 +0100</pubDate>
            <guid isPermaLink="false">609278</guid>        </item>
        <item>
            <title>Acute heart failure: is there a role for surgery?</title>
            <link>http://www.medworm.com/index.php?rid=571144&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj64j6p3j64575638%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Many of the disorders and lesions leading to acute heart failure can be treated surgically. Modern surgical techniques like
 the off pump coronary surgery, newer techniques for the surgical treatment of the mechanical complications of acute MI and
 valvular reparative techniques have been added to the surgical armamentarium in recent years. Modern ventricular assist devices
 have started their career in the clinical arena promising to be less invasive. At the same time the spectrum of indications
 for mechanical circulatory support continues to witness a rapid expansion. Technical advances have led to an evolution of
 surgical strategies. Heart failure surgery is now in a position to offer improved outcomes, avoidance of recurrence of acute
 heart failure or the develop...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=571144</comments>
            <pubDate>Tue, 24 Apr 2007 06:58:44 +0100</pubDate>
            <guid isPermaLink="false">571144</guid>        </item>
        <item>
            <title>Left atrial remodelling contributes to the progression of asymptomatic left ventricular systolic dysfunction to chronic symptomatic heart failure</title>
            <link>http://www.medworm.com/index.php?rid=571145&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fkt4037q86128l485%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Systolic heart failure (HF) is a progressive disorder that often begins with asymptomatic left ventricular (LV) systolic dysfunction
 and culminates in symptoms from fluid overload and poor end-organ perfusion. The progression to symptomatic HF is accompanied
 by marked activation of neurohormonal and cytokine systems, as well as a series of adaptive LV anatomical and functional changes,
 collectively referred to as LV remodelling. However, the mechanisms underlying symptom appearance have not been delineated
 and the weight of experimental and clinical evidence suggests that the development of symptomatic HF occurs independently
 of the haemodynamic status of the patient. The left atrium is a muscular chamber strategically located between the left ventricle
 and the pu...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=571145</comments>
            <pubDate>Sat, 21 Apr 2007 07:08:51 +0100</pubDate>
            <guid isPermaLink="false">571145</guid>        </item>
        <item>
            <title>Epidemiology of acute heart failure syndromes</title>
            <link>http://www.medworm.com/index.php?rid=571146&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fb0505gx5t3k2203n%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Acute Heart Failure is a heterogeneous set of syndromes associated with significant morbidity and mortality. There are several
 classifications of acute heart failure syndromes (AHFS) based on pathophysiology or clinical presentation. In the USA and
 in Europe, AHFS are the first cause of hospitalization of the elderly, and the leading health care cost. Despite this clinical
 and social importance, AHFS have received little attention from clinicians and researchers. Recently published epidemiological
 studies described clinical presentation, characteristics and treatment of over 100,000 patients hospitalized with AHFS. These
 studies also underlined the poor, short, and medium term prognosis, especially for the most severe patients admitted to an
 intensive care unit, w...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=571146</comments>
            <pubDate>Sat, 21 Apr 2007 07:08:50 +0100</pubDate>
            <guid isPermaLink="false">571146</guid>        </item>
        <item>
            <title>Vasodilators in acute heart failure</title>
            <link>http://www.medworm.com/index.php?rid=571148&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F76j5kn2n161t117t%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Most patients with acute heart failure present with increased left ventricular filling pressure and high or normal blood pressure;
 only a minority present with cardiogenic shock. In this context, therapy with vasodilators in the acute setting can improve
 both hemodynamics and symptoms. Vasodilators are usually given in conjunction with diuretics, although much of the acute effect
 of loop diuretics may be due to venodilation. Currently available agents include nitroglycerin, nitroprusside, and nesiritide.
 Nitroglycerin relieves pulmonary congestion primarily through direct venodilation, but may dilate coronary arteries and increase
 collateral blood flow at higher doses, an effect desirable in patients with ischemia. Tachyphylaxis may develop, necessitating
 incremen...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=571148</comments>
            <pubDate>Fri, 20 Apr 2007 07:09:30 +0100</pubDate>
            <guid isPermaLink="false">571148</guid>        </item>
        <item>
            <title>Therapeutic and diagnostic role of electrical devices in acute heart failure</title>
            <link>http://www.medworm.com/index.php?rid=571147&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx8652567n541650q%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Electrical devices, Cardiac Resynchronization Therapy (CRT) pacemakers, the Implantable Cardiac Defibrillator (ICD) and a
 combination of both, constitute an important line of treatment in the therapy of moderate to severe chronic heart failure.
 The effectiveness of these devices in the treatment of acute decompensated heart failure has yet to be systematically evaluated.
 However, the beneficial clinical effects of CRT translate into a marked reduction of heart failure-related hospitalization.
 Devices also offer unique diagnostic applications by continuous measurement of clinically useful physiological parameters
 over time. Of particular interest, monitoring of intrathoracic impedance and right ventricular pressures allows to detect
 changes in volume load in an ear...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=571147</comments>
            <pubDate>Fri, 20 Apr 2007 07:09:30 +0100</pubDate>
            <guid isPermaLink="false">571147</guid>        </item>
        <item>
            <title>Diuretics for the treatment of acute decompensated heart failure</title>
            <link>http://www.medworm.com/index.php?rid=571150&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fn410w764r3451243%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Diuretics have been a mainstay for the treatment of acute decompensated heart failure (ADHF) for the past four decades, though
 their short-term gains have been questioned recently given their potential long-term deleterious systemic effects. The methods
 of diuretic administration as well as the optimal dosing regimen of these agents are both areas that have been increasingly
 coming under scrutiny. The lack of rigorous clinical trials examining diuretic use in ADHF, however, has led to a general
 adoption of non-evidence based treatment algorithms for this patient population. Though the use of intravenous vasodilators
 for the treatment of decompensated heart failure has grown tremendously over the last few years, the fact remains that diuretics
 are still indispensab...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=571150</comments>
            <pubDate>Fri, 20 Apr 2007 07:09:29 +0100</pubDate>
            <guid isPermaLink="false">571150</guid>        </item>
        <item>
            <title>Haemodynamic monitoring in acute heart failure</title>
            <link>http://www.medworm.com/index.php?rid=571149&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fe53473g8x7h604vn%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Acute Heart Failure is a major cause of hospitalisation, with a rate of death and complications. New guidelines have been
 developed in order to diagnose and treat this disease. Despite these efforts pathophysiology and treatments options are still
 limited. There is agreement among the experts that increasing the cardiac output and the stroke volume without fluid overloading
 the patient should be the goal of every treatment. Despite this, there is no agreement on how to monitor the cardiac function
 and how to follow it after a therapeutic intervention. In other fields of critical care cardiovascular monitoring and application
 of early goal directed protocols showed benefits. This review explores the available possibilities of how to monitor the cardiac
 function in ...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
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            <pubDate>Fri, 20 Apr 2007 07:09:29 +0100</pubDate>
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            <title>Algorithm for therapeutic management of acute heart failure syndromes</title>
            <link>http://www.medworm.com/index.php?rid=554714&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fy5552j86847u2x2w%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;As for other critically ill diseases, two key factors may markedly improved morbidity and mortality of acute heart failure
 syndromes (AHFS): early initiation of treatment and tailored therapy. Early initiation aims to stop the negative cascade of
 heart dysfunction. Tailored therapy should be based on the level of systolic blood pressure at admission and fluid retention.
 Indeed, EFICA and OPTIMIZE-HF showed that patients with high systolic blood pressure have a left ventricular systolic function
 that is likely preserved and those with low systolic blood pressure have a lower left ventricular ejection fraction and frequent
 signs of organ’s hypoperfusion. Among the proposed treatments, non-invasive ventilation is the only treatment that was consistently
 proven to b...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
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            <pubDate>Wed, 18 Apr 2007 14:17:01 +0100</pubDate>
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            <title>Natriuretic peptides and therapeutic applications</title>
            <link>http://www.medworm.com/index.php?rid=554715&amp;cid=s_33396_7_f&amp;fid=33396&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fp855171614m80772%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Since the discovery of atrial natriuretic factor by de Bold et&amp;nbsp;al., there has been tremendous progress in our understanding
 of the physiologic, diagnostic and therapeutic roles of the natriuretic peptides (NPs) in health and disease. Natriuretic
 peptides are endogenous hormones that are released by the heart in response to myocardial stretch and overload. Three mammalian
 NPs have been identified and characterized, including atrial natriuretic peptide (ANP or atrial natriuretic factor), B-type
 natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). In addition, Dendroaspis natriuretic peptide (DNP) has been isolated from the venom of Dendroaspis angusticeps (the green mamba snake), and urodilatin from human urine. These peptides are structurally similar...</description>
            <author>Heart Failure Reviews</author>
            <type>journals</type>
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            <pubDate>Wed, 18 Apr 2007 14:16:59 +0100</pubDate>
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